Recently a Harvard study concluded that potatoes are bad for
those wanting to lose weight and be healthy. But is this true
and accurate? Or another example of shoddy "science?" Well, if
we are discussing French Fries, Potato Chips, and the standard
versions of mashed, boiled and baked potatoes (covered with
cheese, butter, bacon and sour cream) then yes, the potato looks
like "bad news." However, if we are talking about the plain old
baked potato (which the FAO/WHO dedicated 2008 to the potato
because of its nutritional and economical value), then no, this
study has no impact on that.

A guideline is suggested for how to read food labels for
grain products such as bread and breakfast cereals. I love doing
these practical day-to-day decision type videos. If you go to
the grocery store and find products that fit the 5 to 1 ratio
rule, please share them in a comment below. They arenít easy to
find!

The U.S. Food and Drug Administration has
approved two new warnings for prescription weight-loss drug Xenical and over-the-counter
pill Alli, making it clear to consumers that both drugs have had reports of severe liver
injury.

Didier Raoult cautions that the use of
probiotics as growth promoters in the farming industry means that further studies should
be carried out before they are regarded as safe for use in humans.

Recent studies on the human gut
microbiota have shown that obesity is associated with a reduction in Gram-negative
bacteria, specifically members of the Bacteroidetes, and an increase in Gram-positive
Firmicutes1. Additionally, it has been shown that the gut microbiota of obese individuals
is less diverse than that of non-obese individuals2. The manipulation of the gut
microbiota  through the administration of probiotics and antibiotics  has been
used for growth promotion in farm animals for 50 years and is regulated by the Food and
Drug Administration (FDA) in the United States and by the European Commission in Europe.
The probiotics used for this purpose in the farming industry include products containing
Firmicutes, in particular Lactobacillus spp., Bifidobacterium spp. and Enterococcus spp.
These products have been marketed and used in most of the animal farming industry,
including in the production of poultry, calves and pigs, and many studies have shown
increases in the size and weight of the young animals that are given these bacterial
additives. Antibiotics have also been used for this purpose, although this practice is now
banned in Europe.

Firmicutes are also used directly as
therapeutic adjuvants in humans, under the names probiotics, prebiotics or, more
generally, 'functional foods'. In the United States, these products are categorized by the
FDA as 'generally regarded as safe' (GRAS; ironically, 'gras' translates as 'fat' in
French). Analysis of these products showed that they contain high concentrations of live
Lactobacillus spp. and Bifidobacterium spp. (up to 108 organisms per gram or millilitre).
These concentrations are similar to those used in animals as growth promoters. In the
United States, probiotic-containing products such as dairy drinks or yogurts typically
contain >107 lactobacilli. Lactobacillus acidophilus is found in functional foods in
amounts that are equivalent to those used to cause weight gain in piglets. Lactobacillus
spp. have also been associated with weight gain in children treated for diarrhoea3. In
addition, some studies have demonstrated weight increases in children who received
Lactobacillus rhamnosus, independent of the disease for which this probiotic was
prescribed4. When these data are considered in the context of the epidemic of childhood
obesity that is occurring in many developed countries, it seems essential to quickly and
more completely study the effects of probiotics in the paediatric population.

Functional foods, including fermented
dairy products containing probiotics, are gaining popularity in many countries, among
children in particular, but little research has been carried out on the connection between
these products and weight gain. These food products are often sold under the guise of
having positive effects on children's health, but there are little conclusive data to
support these claims. Surprisingly, the level of regulation for the use of probiotics in
humans is less strict than that for their use in animals. The specific bacterial species
involved and the concentrations at which they are present are often not made clear to
consumers, and to my knowledge the long-term effects of probiotics as human food
supplements or as adjunctive therapy have never been rigorously evaluated. In my opinion,
further work using experimental models should be carried out to evaluate the role of these
products as animal growth promoters before they are recommended for use in children.

"...further work using
experimental models should be carried out to evaluate the role of these products as animal
growth promoters before they are recommended for use in children."

It is my view that there is a danger
that we may be causing a real human health problem by promoting for human consumption
products containing bacteria that have been associated with weight gain in the animal food
industry. Any chemical compound with such a side effect in experimental animals would be
rigorously tested before being allowed to be used in food. I think that before probiotic
and prebiotic products can be regarded as safe, it is imperative that they are tested in
experimental models that evaluate the propensity of these products to cause obesity in
humans.

Recent studies have revealed that cutting
calories to lose weight raises cortisol, a hormone known to interfere with thyroid
hormones and insulin, cause leptin resistance, and more. High-protein, low-carbohydrate
diets are also thought to consistently raise cortisol levels as well. All of this
contributes to weight gain long-term, regardless of short-term apparent success. Diets
make you fat.

180 Metabolism Weight Loss Audio
Seminar

Boost your metabolism with Matt Stone and
lose weight with this audio series on key elements of successful long-term weight loss.

Barry Groves PhD. discusses the scientific
evidence that supports the use of a low carbohydrate diet for weight loss and reveals
clear evidence why a high carbohydrate diet may be contributing to our obesity crisis.

How obesogens, chemicals in your food and
your environment, make you fat. Dr. Mehmet C. Oz, MD with Dr. Robert Lustig, MD and
Stephen Perrine, Editor-at-Large of Men's Health magazine and author of the book, The New
American Diet. These chemicals include

Fructose

High fructose corn syrup (HFCS)

Bisphenol A (BPA)

PVC (Polyvinyl chloride) which contains
Phthalates

Perfluorooctanoic acid (PFOA), also known as
C8 or perfluorooctanoate found in non-stick coating like teflon coating

Pesticides found in foods such as farmed
salmon

Atrazine,
2-chloro-4-(ethylamino)-6-(isopropylamin≠o)-s-triazine, which is an herbicide that ends
up in our water supply

Fungicides such as tributyltin

Robert Lustig, MD is Professor of Clinical
Pediatrics, in the Division of Endocrinology Director of the Weight Assessment for Teen
and Child Health (WATCH) Program at the University of California, San Francisco, UCSF.

The deleterious effects of fat have been
measured in the presence of high carbohydrate. A high fat diet in the presence of high
carbohydrate is different than a high fat diet in the presence of low carbohydrate.

Watch as Isabel explains how protein
containing foods are an essential part of any fat loss meal plan. Are you eating enough
protein? Are you eating too much protein? Are you eating protein at the right times? Watch
this video to find the answers. Isabel's healthy meal plans and weight loss strategies
have already helped thousands of people not only lose weight, but take complete control of
their health.

We really need to reduce our stress because
our bodies our suffering from adrenal fatigue as we keeping shooting out the hormone
cortisol until it makes us fat. In this video I'm giving you some great ways to reduce
stress so that you can keep your cortisol levels at bay so you don't gain weight and
become fat. Adrenal fatigue is hitting a lot more people today and it can really offset
your life as it makes you fat and reduces your energy levels from all the cortisol being
released from stress.

Stephen Perrine, author of "The New
American Diet," spoke to Harry Smith about certain chemicals found in common foods
called "obesogens" and how they play a role in the American obesity crisis.

Kan een lowcarb dieet je gek maken?

Q. Hi Anthony, I read your They're All MAD!
ebook recently, nice work! You do an excellent job of showing how personal prejudice and
blind dogma determine so much of what is presented to the public as 'scientific' diet and
health information. Thanks for making it freely available.

Your experiences with the low-carb "MAD" movement got me thinking: I remember
you wrote years ago about a study comparing the cognitive effects of a ketogenic low
carb-diet with a non-ketogenic diet, and how the keto diet showed negative effects. Have
you come across any more research on this? I can't help but wonder if the weird behavior
demonstrated by so many online low-carb followers is related to the diet they follow.

A. Great question - and after my experiences with the online low-carb 'community' and a
certain of their incoherent 'gurus', I couldn't help but wonder the same thing. These
people seem to have a far greater than normal capacity for denying reality, and for going
off like a wayward firecracker when someone presents views that contradict their cherished
dogma. And their penchant for performing all manner of mental contortionism in order to
rationalize scientifically untenable beliefs would garner envy from even the most
fanatical Creationist.

Is this a case of the diet causing people to behave irrationally, or irrational people
being attracted to this style of eating?

A persons level of vitamin D may actually
be a predictor of his or her ability to lose fat, according to Shalamar Sibley, a
researcher in the University of Minnesota Medical School. In a clinical study of 38
people, Sibley found that higher baseline levels of vitamin D predicted fat loss,
especially in the abdominal area. The research suggested that if you start out with an
inadequate vitamin D level, its possible that this might inhibit or impede your ability to
lose weight on a reduced caloric diet.

Video - Do low
fat foods make you fat?Do you have to follow a low
fat diet in order to lose weight? The answer might surprise you as you discover the true
value of those supposedly low fat foods. Some food items marked as "healthy"
such as low fat yoghurts often have more energy than unsweetened full fat versions. This
begs the question, is the low fat food market one of the drivers of the obesity epidemic?
View the one hour lecture from UniSA's Gift of Knowledge 2009 lecture series.

Video -
Starvation "Diets" Make You FatYou wanna gain weight, er,
fat? Drastically cut your calorie intake and start fasting. That's how you pack on fat.
Send your body into "Starvation mode" and you'll pack on that fat. In preparing
itself to live through this starvation period, your body does everything it can to protect
the heart. That means turning muscle and lean fiber and everything else into fat to
protect the bodes organ for the long haul.

Video - Killer
at Large Obesity rates in the United
States have reached epidemic proportions in recent years. The Centers for Disease Control
estimate that at least 110,000 people die per year due to obesity and 1/3 of all cancer
deaths are directly related to it. Former Surgeon General Richard Carmona remarked that
obesity is a more pressing issue than terrorism, 'Obesity is a terror within. It's
destroying our society from within and unless we do something about it, the magnitude of
the dilemma will dwarf 9/11 or any other terrorist event that you can point out...' From
our human evolution and our changing environment to the way our government's public
policies are actually causing obesity, Killer at Large shows how little is being done and
more importantly, what can be done to reverse it. Killer at Large also explores the human
element of the problem with portions of the film that follow a 12-year old girl who has a
controversial liposuction procedure to fix her weight gain and a number of others
suffering from obesity, including filmmaker Neil Labute. The film features interviews and
covers events with such notable public figures as Former President Clinton, Ralph Nader,
Senators Tom Harkin and Sam Brownback, Arnold Schwarzenegger, former Surgeon General
Richard Carmona and a number of bestselling authors and renowned experts like Michael
Pollan, Barry Glassner (Bowling for Columbine), Dr. Kelly Brownell (Supersize Me), Dr.
Barry Popkin (Penn and Teller's Bullshit) and many others.

Secret to Effective Dieting?
Portion Control - David Kessler

Former FDA commissioner David Kessler
argues that eating, even while trying to lose weight, must be pleasurable and rewarding.
Dr. Kessler argues for moderation and portion control. There's no "magic
bullet," he says. Drawing on years of extensive research and interviews with medical
experts and industry insiders, former FDA commissioner David. A Kessler tears the brightly
colored packaging off the food business to reveal the startling cultural, biological and
psychological influences that have produced a nation of people hardwired to overeat.
The more hooked on these foods we become, the more of them we will buy. -
Commonwealth Club of California David A. Kessler, M.D., is the Dean of the School of
Medicine and the Vice Chancellor for Medical Affairs at the University of California, San
Francisco. Prior to this appointment, Dr. Kessler served for six years as the Dean of the
Yale University School of Medicine. Dr. Kessler, who served as Commissioner of the Food
and Drug Administration from November 1990 until March 1997, was appointed by President
George H. W. Bush and reappointed by President Clinton. As Commissioner of the FDA, he
acted to speed approval of new drugs and placed high priority on getting promising
therapies for serious and life-threatening diseases to patients as quickly as possible. He
introduced changes in the device approval process to make it more efficient and ensure
that it meets high standards. Under his direction, the FDA announced a number of new
programs, including: user fees for drugs and biologics; the regulation of the marketing
and sale of tobacco products to children; and preventive controls to improve food safety.

Jeffrey Friedman, winner of this year's
Shaw Prize in Life Science and Medicine and Keio Medical Science Prize, discusses his
nearly three decades of research on obesity. Dr. Friedman discovered leptin, a hormone
that regulates food intake and energy expenditure.

The U.S. Food and Drug Administration
announced today that it is reviewing adverse event reports of liver injury in patients
taking the weight loss drug orlistat, marketed as the prescription drug Xenical and the
over-the-counter medication Alli. Between 1999 and 2008, the FDA received 32 reports of
serious liver injury in patients taking orlistat. Of those cases, 27 reported
hospitalization and six resulted in liver failure. Thirty of the adverse events occurred
outside the United States. The most commonly reported adverse events included yellowing of
the skin or whites of the eyes (jaundice), weakness, and stomach pain. The FDA is
reviewing additional data submitted by orlistat manufacturers on suspected cases of liver
injury, and the issue has been discussed at the FDAs Center for Drug Evaluation and
Research Drug Safety Oversight Board. The issues here are complex, but FDA has
benefited from the input of the Board, including comments from representatives from three
FDA Centers and several other Agencies in the Department of Health and Human
Services, said Steven Osborne, M.D., executive director of the Board. The FDAs
analysis of these data is ongoing, and no definite association between liver injury and
orlistat has been established at this time. Consumers taking Xenical should continue to
take it as prescribed, and those using over-the-counter Alli should continue to use the
product as directed.

Full text of the Early Communication
about an Ongoing Safety Review can be found here.
The Early Communication is a risk communication tool used by the FDA to inform the public
about its ongoing safety reviews of drugs. The FDA will release its findings on orlistat
as soon as the review is completed. Consumers who have used orlistat should consult a
health care professional if they experience symptoms possibly associated with development
of liver injury, particularly weakness or fatigue, fever, jaundice, or brown urine. Other
symptoms may include abdominal pain, nausea, vomiting, light-colored stools, itching, or
loss of appetite.

The FDA urges both health care
professionals and consumers to report suspected side effects from the use of orlistat to
FDA's MedWatch Adverse Event Reporting program either online, or by regular mail, fax, or
phone.
-- Online
--Regular Mail: use postage-paid FDA form 3500 and mail to MedWatch, 5600 Fishers Lane,
Rockville, MD 20852-9787
--Fax: 800-FDA-0178
--Phone: 800-FDA-1088

Brainwashing: The Key to Weight
Loss? - Elizabeth Loftus

Elizabeth Loftus discusses her
psychological work using false memories to influence food choices. By embedding a false
food experience, Loftus found subjects avoided fattening foods after being convinced the
food caused them to be extremely sick.

Is Cardio Sabotaging Your Weight
Loss Program?

Get Lean with Glutamine

Glutamine is essential for protein synthesis and fat loss. In the former case, it promotes
anabolism (muscle building) and in the later it reduces the fat content of your body thus
promoting lean muscle growth.

An oil made of natural fatty acids that is sometimes used as a weight-loss supplement may
need to be paired with hormones or other substances to prevent health problems that can
follow rapid weight loss, a new study suggests. Conjugated linoleic acid (CLA), a compound
naturally found in some meat and dairy products, can reduce body fat in some studies in
humans. But a recent study in mice found that the hormone leptin adds an element of
protection against side effects that can accompany fat loss with CLA.

With obesity reaching epidemic levels, researchers at the Ohio State University Medical
Center are studying a potentially long-term treatment that involves injecting a gene
directly into one of the critical feeding and weight control centers of the brain.
"Obesity significantly increases the risk for diabetes, cardiovascular disease,
stroke and some cancers," says Dr. Matthew During, senior author and professor in
Ohio State Medical Center's department of molecular virology, immunology and medical
genetics. "Our findings represent a promising new treatment for obesity that could
ultimately provide a much safer and more effective approach than some conventional
therapies." Scientists have discovered that a particular gene, BDNF, can result in
improved insulin sensitivity, reduced fat mass and weight loss when active in the
hypothalamus. The findings are published online in the journal Nature Medicine. According
to first author Lei Cao, assistant professor in the department of molecular virology,
immunology and medical genetics, the study involved injecting the BDNF gene in normal
mice, diabetic mice and mice fed with a high fat diet, to determine how the gene transfer
would affect their weight. "The gene was active in the overweight mice, but as they
lost weight the gene expression was essentially 'dialed down,' using a novel RNA
interference approach, thus stopping the weight from continuing to decrease and allowing a
stable target weight to be reached," she says. During indicated that with the initial
results showing great promise, the next step is to obtain the necessary FDA approvals to
begin studying the therapy in humans at OSU Medical Center and other centers around the
country.

Bickel is particularly interested in an intriguing relationship between elevated fat
stores in muscles cells and the bodys ability to utilize insulin, a blood-sugar
regulating hormone. While elevated fat stores can be found in the muscle cells of both
endurance athletes and of people with type 2 diabetes, the athletes are sensitive to
insulin and those with type 2 diabetes are resistant to insulin. This paradox has
not been explained, he said. And, I predict that well find the lipid
droplets within muscles of such athletes will have different coat proteins than those that
coat the lipid droplets of people with type 2 diabetes.

Controlling body weight is a complicated process, as any frustrated dieter might attest.
But as scientists continue to investigate the brains intricate neurocircuitry and
its role in maintaining energy balance, they are forming a clearer picture of the myriad
events that lead to weight gain and weight loss.In the August 10 on-line issue of Nature
Neuroscience, a study led by scientists at Beth Israel Deaconess Medical Center (BIDMC)
identifies another piece of this complex puzzle, demonstrating that the neurotransmitter
GABA --one of the master communicators among neurons  plays a role in controlling
energy balance.

Could sleep be a critical component to maintaining a healthy body weight? According to new
research to be presented on Sunday, May 17, at the American Thoracic Society's 105th
International Conference in San Diego, body mass index (BMI) is linked to length and
quality of sleep in a surprisingly consistent fashion. As part of the Integrative Cardiac
Health Project at Walter Reed Army Medical Center, researchers analyzed the sleep,
activity and energy expenditures of 14 nurses who had volunteered for a heart-health
program at the Walter Reed, where the nurses were employed. The program included
nutritional counseling, exercise training, stress management and sleep improvement. Each
participant wore an actigraphy armband that measured total activity, body temperature,
body position and other indices of activity and rest. "When we analyzed our data by
splitting our subjects into 'short sleepers' and 'long sleepers,' we found that short
sleepers tended to have a higher BMI, 28.3 kg/m2, compared to long sleepers, who had an
average BMI of 24.5. Short sleepers also had lower sleep efficiency, experienced as
greater difficulty getting to sleep and staying asleep," said lead investigator Arn
Eliasson, M.D. Surprisingly, overweight individuals tended to be more active than their
normal weight counterparts, taking significantly more steps than normal weight
individuals: 14,000 compared to 11,300, a nearly 25 percent difference, and expending
nearly 1,000 more calories a day3,064 versus 2,080.

Ear infections are a painful rite of passage for many children. New research suggests the
damage caused by chronic ear infections could be linked to people's preference for fatty
foods, which increases their risk of being overweight as they age. Scientists from around
the country presented their findings on this unexpected connection at the American
Psychological Association's 116th Annual Convention here Thursday.

People who use monosodium glutamate, or MSG, as a flavor enhancer in their food are more
likely than people who don't use it to be overweight or obese even though they have the
same amount of physical activity and total calorie intake, according to a University of
North Carolina at Chapel Hill School of Public Health study published this month in the
journal Obesity. Researchers at UNC and in China studied more than 750 Chinese men and
women, aged between 40 and 59, in three rural villages in north and south China. The
majority of study participants prepared their meals at home without commercially processed
foods. About 82 percent of the participants used MSG in their food. Those users were
divided into three groups, based on the amount of MSG they used. The third who used the
most MSG were nearly three times more likely to be overweight than non-users. "Animal
studies have indicated for years that MSG might be associated with weight gain," said
Ka He, M.D., assistant professor of nutrition and epidemiology at the UNC School of Public
Health. "Ours is the first study to show a link between MSG use and weight in
humans." Because MSG is used as a flavor enhancer in many processed foods, studying
its potential effect on humans has been difficult. He and his colleagues chose study
participants living in rural Chinese villages because they used very little commercially
processed food, but many regularly used MSG in food preparation. "We found that
prevalence of overweight was significantly higher in MSG users than in non-users," He
said. "We saw this risk even when we controlled for physical activity, total calorie
intake and other possible explanations for the difference in body mass. The positive
associations between MSG intake and overweight were consistent with data from animal
studies."

Two studies question the validity
of the BMI in the assessment of health

However, when the researchers started looking at the results of the obese individuals
according to whether they were insulin resistance or not the results became a bit more
revealing. Distinct differences were found between these two types of obese
person. In particular, compared to those who were insulin sensitive, the insulin
resistance individuals were found to have significantly more fat in their livers and
thicker arteries.

Sick of the same old thing? U of
Minnesota researcher finds satiation solution

Have you ever gotten sick of pizza, playing the same computer game, or had a song stuck in
your head for so long you never wanted to hear it again? If you have, you may suffer from
variety amnesia. In new research, Joseph Redden, professor of marketing at the University
of Minnesota's Carlson School of Management, may have found a cure for your satiation
blues. "People forget about the abundance of different experiences they have had and
tend to focus on the repetition," said Redden. "Simply thinking about the
variety of songs they have listened to or meals they have eaten will make people enjoy the
activity again." Satiation, the process of consuming products and experiences to the
point where they are less enjoyable, is a big problem for consumers and retailers. In the
past, time and variety have been seen as the only ways to cure satiation. In their new
article forthcoming in the Journal of Consumer Research, Redden and co-authors find that
just recalling variety may cure satiation faster. "Intuition says that if time passes
we will like something again: we call this 'spontaneous recovery,' " said Redden.
"This isn't the whole story. People don't fully recover on their own with the mere
passage of time. If I'm sick of chocolate, simply thinking about all the other desserts
I've had since the last time I had chocolate helps cure my satiation. Time doesn't seem to
do that very well." In one of the three studies conducted for this research, Redden
and his co-authors asked participants to listen to the chorus of a favorite song 20 times
in a row. Then they were asked to rate the clip. Not surprisingly, after 20 repetitions
their enjoyment of the song dropped a great deal. Three weeks later, the participants came
back and half were asked to recall any television shows they'd seen since the study, while
the other half listed all of the musicians they'd listened to since the first session. The
group that listed the TV shows was still just as satiated  they didn't like the
song. However, those recalling variety in the music category almost totally recovered.
"The participants' comments were the most revealing," said Redden. "Those
who recalled the TV shows were actually angry to have a song they like 'ruined,' but the
ones who recalled musicians enjoyed taking a study with music, etc. If something seems
like 'more of the same,' people are just less interested."

Boosting calcium consumption spurs weight loss, according to a study published in the most
recent issue of the British Journal of Nutrition, but only in people whose diets are
calcium deficient. Angelo Tremblay and his team at Universitť Lavals Faculty of
Medicine made the discovery in a 15-week weight loss program they conducted on obese
women. The participants consumed on average less than 600 mg of calcium per day, whereas
recommended daily intake is 1000 mg. In addition to following a low calorie diet, the
women were instructed to take two tablets a day containing either a total of 1200 mg of
calcium or a placebo. Those who took the calcium tablets lost nearly 6 kg over the course
of the program, the researchers found, compared to 1 kg for women in the control group.
Our hypothesis is that the brain can detect the lack of calcium and seeks to
compensate by spurring food intake, which obviously works against the goals of any weight
loss program, said Angelo Tremblay, holder of the Canada Research Chair in
Environment and Energy Balance. Sufficient calcium intake seems to stifle the desire
to eat more, he added.

A new study in mice indicates that overeating, rather than the obesity it causes, is the
trigger for developing metabolic syndrome, a collection of heath risk factors that
increases an individuals chances of developing insulin resistance, fatty liver,
heart disease and type 2 diabetes. How and where the body stores excess, unused calories
appears to matter most when determining a persons risk of developing metabolic
syndrome, researchers at UT Southwestern Medical Center suggest. Most people today
think that obesity itself causes metabolic syndrome, said Dr. Roger Unger, professor
of internal medicine at UT Southwestern and senior author of the study. Were
ingrained to think obesity is the cause of all health problems, when in fact it is the
spillover of fat into organs other than fat cells that damages these organs, such as the
heart and the liver. Depositing fatty molecules in fat cells where they belong actually
delays that harmful spillover.

Counting calories that burn through activity is a constant quandary. One can only run on a
treadmill so long, watching intently as the pedometer reads out the number of calories
melted during a session of exercise. Not to mention the question of how many calories are
burned through basic daily movements and even during sleep. But technology  and
youthful ambition  is presenting a round-the-clock solution for those consumed with
this calculation. A group of Georgia Tech students has crafted a device that allows
individuals to constantly compute the amount of calories they burn  even as they
sleep. Its a completely converged device, said Garrett Langley, 21, a
senior in the School of Electrical and Computer Engineering (ECE) who spearheaded the
project. Its a single unit that provides complete fitness monitoring and
management.

Not enough vitamin D in the diet
could mean too much fat on adolescents

Too little vitamin D could be bad for more than your bones; it may also lead to fatter
adolescents, researchers say. A Medical College of Georgia study of more than 650 teens
age 14-19 has found that those who reported higher vitamin D intakes had lower overall
body fat and lower amounts of the fat in the abdomen, a type of fat known as visceral fat,
which has been associated with health risks such as heart disease, stroke, diabetes and
hypertension. The group with the lowest vitamin D intake, black females, had higher
percentages of both body fat and visceral fat, while black males had the lowest
percentages of body and visceral fat, even though their vitamin D intake was below the
recommended levels. Only one group  white males  was getting the recommended
minimum intake of vitamin D. This study was a cross-section so, while it cannot
prove that higher intake of vitamin D caused the lower body fat, we know there is a
relationship that needs to be explored further," says Dr. Yanbin Dong, a molecular
geneticist and cardiologist at the MCG Gerogia Prevention Institute. Dr. Dong, who also
co-directs the MCG Diabetes & Obesity Discovery Institute, and Inger
Stallman-Jorgensen, a research dietician at the GPI, present their findings this week at
the American Heart Associations Joint 49th Conference on Cardiovascular Disease
Epidemiology and Prevention and Nutrition, Physical Activity and Metabolism in Palm
Harbor, Fla.

Phthalates used in food packaging could be linked to childhood obesity, according to two
recent studies conducted by the Mount Sinai School of Medicine that included research
conducted on more than 900 children in East Harlem and surrounding communities. The
studies have added to a growing body of evidence that link phthalates to health problems.

The ETHERPATHS project focuses on the balance of lipid metabolism in the body, the effects
of foods in tissues and the role of gut microbiota in these processes. Lipid metabolism
disorders are associated with several common health care problems, such as ageing,
diabetes and cardiovascular diseases. The balance can be influenced by dietary means. The
risk of chronic diseases decreases with a diet containing particularly omega-3 fatty acids
and foods that contain fibres and phenol. Therefore, fatty fish, berries, fruits and
vegetables may be favourable foods in terms of lipid metabolism balance. The body's own
phospholipids are assumed to mediate the health-promoting effects, but their mechanisms of
action are still unknown.

A surprise discovery -- that calorie-burning brown fat can be produced experimentally from
muscle precursor cells in mice -- raises the prospect of new ways to fight obesity and
overweight, say scientists from Dana-Farber Cancer Institute. Reporting in the Aug. 21
issue of the journal Nature, the researchers demonstrated that brown fat, which is known
as the "good" form of fat -- so called because it burns calories and releases
energy, unlike "bad" white fat that simply stores extra calories -- can be
generated from unspecialized precursors that routinely spawn skeletal muscle. The team led
by Dana-Farber's Bruce Spiegelman, PhD, showed that a previously known molecular switch,
PRDM16, regulates the creation of brown fat from immature muscle cells. They also
determined that the process is a two-way street: Knocking out PRDM16 in brown fat cells
can convert them into muscle cells. However, Spiegelman called the latter an
"experimental lab trick" for which he currently envisions no practical
applications. The "huge surprise" of the study results, he said, was that muscle
precursor cells known as "satellite cells" are able to give birth to brown fat
cells under the control of PRDM16. Spiegelman said the finding confirms that PRDM16 is the
"master regulator" of brown fat development. The confirmation will spur ongoing
research in his laboratory, he said, to see if drugs that rev up PRDM16 in mice -- and
potentially, in people -- could convert white fat into brown fat and thereby treat
obesity. Another strategy, he said, might be to transplant brown fat cells into an
overweight person to turn on the calorie-burning process.

It's not just sugary sodas that are adding to the obesity crisis -- it's fruit drinks,
alcohol and a combination of other high-calorie beverages, say University of North
Carolina at Chapel Hill School of Public Health researchers. And during the holidays, when
eggnog, cocktails and spiced cider are abundant, the problem can be even more apparent.

A study by researchers at the Joslin Diabetes Center has shown that a protein known for
its role in inducing bone growth can also help promote the development of brown fat, a
"good" fat that helps in the expenditure of energy and plays a role in fighting
obesity. "Obesity is occurring at epidemic rates in the U.S. and worldwide and that
impacts the risk and prognosis of many diseases," said Yu-Hua Tseng, Ph.D. an
Assistant Investigator in the Joslin Section on Obesity and Hormone Action and lead author
of the paper published in the August 21 issue of Nature. "We hope this study can be
translated into applications to help treat or prevent obesity." Tseng noted that
obesity is a major risk factor for type 2 diabetes and is closely linked to the metabolic
syndrome, a collection of medical problems associated with insulin resistance that can
lead to an increased risk of atherosclerosis, the buildup of plaque in coronary arteries
that leads to heart attack and stroke. In laboratory studies of mouse cells, Tseng and her
colleagues identified that a bone-inducing protein called BMP-7 drives precursor cells
that give rise to mature brown fat cells. According to Tseng, there are two main types of
fat cells in the body  white and brown. "White fat cells are the 'conventional'
form of fat designed to store energy. By contrast, the main role of brown fat is to burn
calories by generating heat. Brown fat cells largely disappear by adulthood in humans, but
their precursors still remain in the body," Tseng explained. A 2005 Joslin study by
Dr. Tseng and colleagues discovered genes that control the creation of the precursor cells
of brown fat. Another more recent 2007 Joslin study led by C. Ronald Kahn, M.D., head of
the Joslin Section on Obesity and Hormone Action and also a co-author of the current
Nature study, found clusters of brown fat cells dispersed between bundles of muscle fibers
in an obesity-resistant strain of mice. Now, this latest study identified BMP-7 as the
protein capable of inducing the formation and function of brown fat cells. According to
the paper, delivery of BMP-7 into mice using adenovirus as a vector resulted in an
increase in the development of brown fat tissue. In one of the experiments, the mice that
developed brown fat tissue gained less weight than those that did not. In another
experiment, mice that received injections of progenitor cells  similar to stem cells
 that had been pre-treated with BMP-7 also developed additional brown fat tissue.

Scientists at the Gladstone Institutes of Cardiovascular Disease (GICD) have found that a
key enzyme involved in absorbing fat may also be a key to reducing it. The enzyme, acyl
CoA: monoacylglycerol acyltransferase 2 or Mgat2 is found in the intestines and plays an
important part in the uptake of dietary fat by catalyzing a critical step in making
triglyceride, a kind of fat. Triglyceride accounts for nearly one-third of the fat eaten
by people in developed countries. Researchers in the laboratory of Robert V. Farese, Jr.
MD, found that mice that were genetically modified to lack Mgat2 remain normal on a
low-fat diet. However, when fed a high-fat diet that is similar to that eaten by many
Americans, the mice do not get fat and do not develop other symptoms of obesity, such as
glucose intolerance, hypercholesterolemia, and fatty livers. The mice eat the same number
of calories as other mice, and the calories are fully absorbed. Results of their study
were published in the current issue of the journal Nature Medicine. "Because mice
that lack this enzyme do not gain weight on a high-fat diet, it is an intriguing target
for future interventions to prevent weight gain and the problems associated with that
extra weight," said Dr. Farese. The mechanism of action, the researchers identified
was that the lack of Mgat2 may reduce the uptake of fat in the small intestine and delay
its entry into the blood. This process may dissociate fat from carbohydrate absorption and
insulin secretion and ultimately lower the amount of fat stored and used. How this happens
is not clear. One possibility is that the absorbed fat is partitioned more to tissues
where it is burned up. "Differences in Mgat2 expression may contribute to the
propensity of some people to gain weight from diets rich in fat," said Eric Yen, PhD,
lead author of the study. "Our findings suggest that inhibiting this enzyme in the
small intestine might be an effective way to treating metabolic diseases that result from
excessive fat intake."

Headlines tell us the nation is getting fatter, and that obesity has become an epidemic.
But there is more to the story, according to one University of Houston sociologist. While
she acknowledges that there has been a shift in body weight over the years, assistant
sociology professor Samantha Kwan looks at obesity from a different perspective. The term
obesity was constructed by the medical community, Kwan says. And the use of the Body Mass
Index, which measures obesity, as the main factor to define obesity, has resulted in the
media greatly overstating the rise of the condition. "This epidemic has been
constructed to the benefit of the medical industry that has in part medicalized the
treatment of obesity over the years," Kwan says. "While there may be a rise in
'obesity,' the BMI is not always accurate. Some scholars describe this epidemic more as a
moral panic. While there may be some truths to rising rates, they have been
overstated." Kwan, who has been studying gender and body image since 2001, examines
how cultural beauty messages about fat interact with other cultural messages about fat,
such as health discourses. This is summarized in her article "Framing the Fat Body:
Contested Meanings between Government, Activists and Industry," published in
February's Sociological Inquiry. "I am trying to get students and audiences to
understand that there are competing cultural meanings about the fat body," Kwan says.
"Fat does not, in itself, signify unhealthy and unattractive. These are cultural
constructions. We as a society say what it means to be fat, and right now cultural
discourses say it's ugly and unhealthy to be fat. It's also assumed that the body
is a reflection of the psyche, including one's moral fiber." Kwan has found that
women's self-esteem is more closely tied to weight than men's.

Most of the current obesity research is not proving helpful in finding solutions to the
growing international epidemic, according to a Deakin University public health expert.
Professor Boyd Swinburn believes that research funding would be better directed at testing
possible solutions rather than continuing to unpick what is causing the rise in obesity.
"It seems counter intuitive, but knowing the causes or mechanisms for weight gain
does not always help with identifying the solutions," he said. "For an
individual person, we know the causes of weight gain over time include the obesogenic
environment, genetic predisposition, and increasing age  none of which can be
influenced by the health professional trying to help the person lose weight. At a
population level, the commercial drivers which promote our overconsumption of food are
unlikely to be reversed by the private sector because there is no commercial gain for the
food industry to promote eating fewer calories. "The twin bottom line is that we need
to re-orient our research towards testing potential solutions rather than just better
identifying the problem. The most promising approaches for individuals and populations
will involve identifying the right set of 'rules' or policies which lead to sustainable
environmental and behavioural changes." Professor Swinburn says that identifying
solutions needs specific solutions-oriented research and unfortunately most of the current
research into obesity is problem-oriented. "Interestingly, the solutions that are the
most likely to work seem to be 'rule-based' solutions," Professor Swinburn explained.

A study published in the May 1 issue of the journal Sleep is the first known to report
that short and long sleepers are more likely to have metabolic syndrome, or a combination
of medical disorders that increase the risk of developing cardiovascular disease.

New Study in the Journal SLEEP
Finds a Consistent, Worldwide Association Between Short Sleep Duration and Obesity in
Children and Adults

A study published in the May 1 issue of the journal SLEEP is the first attempt to quantify
the strength of the cross-sectional relationships between duration of sleep and obesity in
both children and adults. Cross-sectional studies from around the world show a consistent
increased risk of obesity among short sleepers in children and adults, the study found.
Francesco P. Cappuccio, MD, of Warwick Medical School in the United Kingdom, and
colleagues performed a systematic search of publications on the relationship between short
sleep duration and obesity risk. Criteria for inclusion were: report of duration of sleep
as exposure, body mass index (BMI) as continuous outcome and prevalence of obesity as
categorical outcome, number of participants, age and gender.

A University of Navarra study has
revealed that the consumption of fruits and legumes aids in losing more than 6% of body
weight

Foods rich in compounds with antioxidant capacity, such as fruits and legumes, help to
lose more than 6% of body weight when they are included in low-calorie diets for
nutritional treatment of obesity. This conclusion was derived from the doctoral research
of the biologist Ana Belťn Crujeiras, a researcher of the Department of Diet, Physiology
and Toxicology of the University of Navarra. In addition to the effects associated with
weight loss, Dr. Crujeiras added that another consequence of this diet is an improvement
in cholesterol levels thanks to dietary fiber, and a reduction in body fat. This is due to
protection against oxidative stress, a mechanism which underlies the development of
pathologies associated with obesity, including cardiovascular and neurodegenerative
diseases, diabetes, and even cancer, she indicated.

Exposure to insecticide may play
role in obesity epidemic among some women

Prenatal exposure to an insecticide commonly used up until the 1970s may play a role in
the obesity epidemic in women, according to a new study involving several Michigan State
University researchers. More than 250 mothers who live along and eat fish from Lake
Michigan were studied for their exposure to DDE  a breakdown of DDT. The study,
published as an editors choice in this months edition of Occupational and
Environmental Medicine, analyzed DDE levels of the womens offspring. Compared to the
group with the lowest levels, those with intermediate levels gained an average of 13
pounds excess weight, and those with higher levels gained more than 20 pounds of excess
weight. Prenatal exposure to toxins is increasingly being looked at as a potential
cause for the rise in obesity seen worldwide, said Janet Osuch, a professor of
surgery and epidemiology at MSUs College of Human Medicine, who was one of the lead
authors of the study. What we have found for the first time is exposure to certain
toxins by eating fish from polluted waters may contribute to the obesity epidemic in
women. Though DDT was banned in 1973 after three decades of widespread use, the
chemical and its byproducts remain toxic in marine life and fatty fish. The study was
funded by a $300,000 grant from the federal Agency for Toxic Substances and Disease
Registry. Osuch said the studys findings can have a huge impact on how researchers
treat  and seek to prevent  obesity. The research team has been awarded a $1
million grant from the same federal agency, the ATSDR, to assess the impact of pollutants
and toxins on a wide variety of disorders by determining the importance of second- and
third-generation health effects.

Conventional wisdom says that the meteoric rise in obesity and related health conditions -
the early stages of which are now called metabolic syndrome - is due to the West having a
bad case of "couch potato syndrome." That is, over the past few decades, we have
been eating too much and not exercising enough. While poor diet and inactivity play an
undeniable role in fostering metabolic syndrome, that's not the whole story. Clinical and
epidemiological evidence increasingly implicates another culprit: the environment. An
insufficient explanation Some scientists suspect that a combination of environmental
factors, including a group of chemicals called obesogens, share the blame for the
explosion of metabolic syndrome and its later stages: diabetes, obesity, cardiovascular
disease, and even Alzheimer's. "Despite what we've heard," said Dr. Bruce
Blumberg, Professor of Developmental and Cell Biology and Pharmaceutical Sciences at the
Univeristy of California, Irvine, "diet and exercise alone are insufficient to
explain the obesity epidemic."

A Temple University study finds fat in obese patients is sick when compared to
fat in lean patients. When our bodies dont work properly, we say were sick. A
study published in the September issue of Diabetes finds that the same could be said for
fat tissue found in obese patients. The cells in their fat tissue arent working
properly and as a result, are sicker than cells found in lean patients fat tissue.
Lead author Guenther Boden, M.D. theorizes that sick fat could more fully
explain the link between obesity and higher risk of diabetes, heart disease and stroke.
Researchers from the departments of endocrinology, biochemistry and surgery at the Temple
University School of Medicine took fat biopsies from the upper thighs of six lean and six
obese patients and found significant differences at the cellular level. The fat
cells we found in our obese patients were deficient in several areas, said Boden,
Laura H. Carnell Professor of Medicine and chief of endocrinology. They showed
significant stress on the endoplasmic reticulum, and the tissue itself was more inflamed
than in our lean patients.

Low Levels of Brain Chemical May
Lead to Obesity, NIH Study of Rare Disorder Shows

A brain chemical that plays a role in long term memory also appears to be involved in
regulating how much people eat and their likelihood of becoming obese, according to a
National Institutes of Health study of a rare genetic condition. Brain derived
neurotrophic factor (BDNF) is, as its name implies, produced in the brain. Studies of
laboratory animals have suggested it also helps control appetite and weight. The NIH
study, appearing in the August 28 New England Journal of Medicine, provides the first
strong evidence that BDNF is important for body weight in human beings as well. The NIH
researchers studied children and adults with WAGR syndrome, a rare genetic condition. The
researchers found that some of the people with this syndrome lack a gene for BDNF and have
correspondingly low blood levels of the substance. The people in this subgroup also have
unusually large appetites and a strong tendency towards obesity. This is a promising
new lead in the search for biological pathways that contribute to obesity, said
Duane Alexander, M.D., director of the NIHs Eunice Kennedy Shriver National
Institute of Child Health and Human Development. This finding may eventually lead to
the development of new drugs to regulate appetite in people who have not had success with
other treatments. The studys first author was Joan C. Han, M.D. and the senior
author was Jack A. Yanovski, M.D., Ph.D., both of NICHDs Unit on Growth and Obesity.
Other authors of the study were from the National Human Genome Research Institute and the
National Institute on Drug Abuse, also part of the NIH. Funding for the study was provided
by the NICHD and the NIH Office of Rare Diseases.

New master switch found in the
brain that regulates appetite and reproduction

Body weight and fertility have long known to be related to each other  women who are
too thin, for example, can have trouble becoming pregnant. Now, a master switch has been
found in the brain of mice that controls both, and researchers at the Salk Institute for
Biological Studies say it may work the same way in humans.Findings from the study,
published ahead of print in the Aug. 31 online edition of Nature Medicine, suggest that
variations in the gene that produces this master switch, known as TORC1, could contribute
a genetic component to obesity and infertility, and might be regulated with a novel drug.
"This gene is crucial to the daisy chain of signals that run between body fat and the
brain," says Marc Montminy, Ph.D., a professor in the Clayton Foundation Laboratories
for Peptide Biology, who led the study. "It likely plays a pivotal role in how much
we, as humans, eat and whether we have offspring."It is just as important as leptin,
the well-known star regulator of appetite, Montminy says, because leptin turns on TORC1,
which in turn activates a number of genes known to help control feeding and fertility.
Judith Altarejos Ph.D., first author on this study, had been trying to understand human
energy balance, and what can go awry to promote obesity, diabetes and other metabolic
syndromes. In this study, she looked at the signals that travel from body fat to the
brain, informing the brain of how well fed the body is. The primary hormone that performs
that function is leptin, which travels through the bloodstream to the hypothalamus in the
brain (the appetite center), keeping the brain aware of the body's nutritional status.
"Leptin tells the brain that times are good, your body is full, and that it is not
necessary to eat more at the moment," Montminy says. The hormone also is known to
play a role in reproduction - although, until this study, no one understood what is was.
(Very thin women often do not have periods.) "Controlling appetite and reproduction
together provides a big evolutionary advantage," Montminy says. "If there is no
food, the brain believes the body should not reproduce because without body fat, a baby's
growth in the womb could be stunted, and without food to replenish the body's energy
reserves, there will be nothing to feed the offspring." "Leptin works remarkably
well to give the brain a good indication of how much food has been eaten; 99.9 percent of
the time it balances food intake with energy use," he says. "The problem is that
no machine works 100 percent of the time, and that slight bit of inefficiency can lead to
extra body weight." Obesity results when the brain becomes "deaf" to the
leptin signal, so one goal of Montminy's research is to "try to make a way to make
sure the brain signals are being heard." But to do that, he and his research team
first have to understand all of the signals involved in the satiety pathway. Through years
of research, they have uncovered a family of genes that act as energy switches, turning
other genes on or off. One gene, TORC2, acts like a fasting switch that flips on the
production of glucose in the liver when blood glucose levels run low, usually during
sleep. During the day, the hormone insulin normally shuts down TORC2, ensuring that blood
sugar levels don't rise too high. Problems along the pathway, however, can help lead to
diabetes.

It's the French paradox redux: Why don't the French get as fat as Americans, considering
all the baguettes, wine, cheese, pate and pastries they eat? Because they use internal
cues -- such as no longer feeling hungry -- to stop eating, reports a new Cornell study.
Americans, on the other hand, tend to use external cues -- such as whether their plate is
clean, they have run out of their beverage or the TV show they're watching is over.

Conducted by researchers at the Manchester Metropolitan University, the new study, has
found that exercise, low to moderate workouts, and a diet containing proteins and
carbohydrates can help old people live longer and stay healthier.

It is amazing how the little twists and turns of researchers can have such a profound
impact on what we generally come to realize as scientific truth. Let me share
a recent fascinating example of how this impacted one of the most powerful hormones in
your body.

Johns Hopkins scientists report success in significantly suppressing levels of the
hunger hormone ghrelin in pigs using a minimally invasive means of chemically
vaporizing the main vessel carrying blood to the top section, or fundus, of the stomach.
An estimated 90 percent of the bodys ghrelin originates in the fundus, which
cant make the hormone without a good blood supply. With gastric artery
chemical embolization, called GACE, theres no major surgery, says Aravind
Arepally, M.D., clinical director of the Center for Bioengineering Innovation and Design
and associate professor of radiology and surgery at the John Hopkins University School of
Medicine. In our study in pigs, this procedure produced an effect similar to
bariatric surgery by suppressing ghrelin levels and subsequently lowering appetite.
Reporting on the research in the September 16 online edition of Radiology, Arepally and
his team note that for more than a decade, efforts to safely and easily suppress grehlin
have met with very limited success.

New study reveals higher protein
breakfast may help dieters stay on track

A new study published online today in the British Journal of Nutrition found that timing
of dietary protein intake affects feelings of fullness throughout the day. The study
concluded that when people ate high-quality protein foods, from sources such as eggs and
lean Canadian bacon, for breakfast they had a greater sense of sustained fullness
throughout the day compared to when more protein was eaten at lunch or dinner. "There
is a growing body of research which supports eating high-quality protein foods when
dieting to maintain a sense of fullness," said Wayne W. Campbell, PhD, study author
and professor of Foods and Nutrition at Purdue University. "This study is
particularly unique in that it looked at the timing of protein intake and reveals that
when you consume more protein may be a critical piece of the equation." The study
included overweight or obese men who ate a reduced calorie diet. The diet consisted of two
variations of protein intakes, both which were within federal nutrition recommendations:
normal protein intake (11-14 percent of calories) or increased protein (18-25 percent of
calories). The researchers tested the effect of consuming the additional protein at
specific meals  breakfast, lunch or dinner  or spaced evenly throughout the
day. Purdue researchers found that the feeling of fullness was greatest and most sustained
throughout the day when the additional protein, from eggs and lean Canadian bacon, was
eaten at breakfast  versus lunch or dinner.

Cross-sectional studies have reported an association between major depressive episode
(MDE) and obesity. The objective of this longitudinal analysis was to determine whether
MDE increase the risk of becoming obese over a 10-year period. Data from the Canadian
National Population Health Survey (NPHS) were used, a longitudinal study of a
representative cohort of household residents in Canada. The incidence of obesity, defined
as a body mass index (BMI) of 30, was evaluated in respondents who were 18 years or older
at the time of a baseline interview in 1994. MDE was assessed using a brief diagnostic
instrument. At the end of the investigation, the risk of obesity was not elevated in
association with MDE, either in unadjusted or covariate-adjusted analyses. The strongest
predictor of obesity was a BMI in the overweight (but not obese) range. Effects were also
seen for (younger) age, (female) sex, a sedentary activity pattern, low income and
exposure to antidepressant medications. Unexpectedly, significant effects were seen for
serotonin-reuptake-inhibiting antidepressants and venlafaxine, but neither for tricyclic
antidepressants nor antipsychotic medications.

Researchers from the UGR have analysed the diet followed by thirty students aged between
19 and 27 during Ramadan. They tested that the diet led to an increase in corporal fat and
a reduction in muscular mass. They suggest modifications in diet to reduce fat and
increase proteins and carbohydrates, according to the nutritional needs of this population
group.

New research from the University of Cincinnati (UC) implicates the primary chemical used
to produce hard plasticsbisphenol A (BPA)as a risk factor for metabolic
syndrome and its consequences. In a laboratory study, using fresh human fat tissues, the
UC team found that BPA suppresses a key hormone, adiponectin, which is responsible for
regulating insulin sensitivity in the body and puts people at a substantially higher risk
for metabolic syndrome. Metabolic syndrome is a combination of risk factors that include
lower responsiveness to insulin and higher blood levels of sugar and lipids. According to
the American Heart Association, about 25 percent of Americans have metabolic syndrome.
Left untreated, the disorder can lead to life-threatening health problems such as coronary
artery disease, stroke and type 2 diabetes. Nira Ben-Jonathan, PhD, and her team are the
first to report scientific evidence on the health effects of BPA at environmentally
relevant doses equal to "average" human exposure. Previous studies have
primarily focused on animal studies and high doses of BPA. They report their findings in
the Aug. 14, 2008, online edition of the journal Environmental Health Perspectives. This
scientific data comes just before a key Federal Drug Administration meeting about the
safety of the chemical in consumer products scheduled for Sept. 16, 2008. "People
have serious concerns about the potential health effects of BPA. As the scientific
evidence continues to mount against the chemical, it should be given serious attention to
minimize future harm," says Ben-Jonathan, a professor of cancer and cell biology at
UC who has studied BPA for more than 10 years.

A Universitť Laval research team has demonstrated that intellectual work induces a
substantial increase in calorie intake. The details of this discovery, which could go some
way to explaining the current obesity epidemic, are published in the most recent issue of
Psychosomatic Medicine. The research team, supervised by Dr. Angelo Tremblay, measured the
spontaneous food intake of 14 students after each of three tasks: relaxing in a sitting
position, reading and summarizing a text, and completing a series of memory, attention,
and vigilance tests on the computer. After 45 minutes at each activity, participants were
invited to eat as much as they wanted from a buffet. The researchers had already shown
that each session of intellectual work requires only three calories more than the rest
period. However, despite the low energy cost of mental work, the students spontaneously
consumed 203 more calories after summarizing a text and 253 more calories after the
computer tests. This represents a 23.6% and 29.4 % increase, respectively, compared with
the rest period.

A group of sedentary and overweight older people placed on a four-month exercise program
became more fit and burned off more fat, compared to older sedentary people who dieted but
did not exercise. The new study also showed that when older people diet without
exercising, they lose more lean muscle compared to those who exercise. When they combined
weight loss with exercise, it nearly completely prevented the loss of lean muscle mass.

The combination of two obesity-related genetic variations may be associated with an
increased body mass index among severely obese patients undergoing bariatric weight loss
surgery, according to a report in the March issue of Archives of Surgery, one of the
JAMA/Archives journals.

Some scientists suspect that a combination of environmental factors, including a group of
chemicals called obesogens, share the blame for the explosion of metabolic syndrome and
its later stages - diabetes, obesity, cardiovascular disease, and even Alzheimers.

Scientists at the Harvard School of Public Health (HSPH) have identified in mice a newly
discovered class of hormones -- lipokines, according to a report in the September 19,
2008, issue of Cell. Furthermore, they have implicated a lipokine as a molecule in mice
that helps stop or even reverse obesity-related conditions such as insulin resistance and
"fatty liver." Lipokines are hormones made from lipids, or fats. All other known
hormones -- chemical signals secreted into the blood that regulate distant cells and
organs -- are steroid- or protein-based. Researchers, led by HSPH Professor GŲkhan
Hotamisligil, knew from previous experiments that an unidentified factor in the fat tissue
of genetically engineered mice sent signals to regulate metabolism in liver and muscle
tissues. The researchers suspected that elucidating the mechanism could be of
significance.

The enzyme TPPII may contribute to obesity by stimulating the formation of fat cells,
suggests a study in EMBO reports this week. The enzyme, TPPII, has previously been linked
to making people feel hungry, but Jonathan Graff and colleagues now show that it may be
even more deeply involved in causing obesity.

The hormone prolactin is necessary for the production of breast milk, but it also affects
adipose (fatty) tissue and the bodys metabolism. This has been shown by a thesis
from the Sahlgrenska Academy, University of Gothenburg, Sweden. Raised prolactin levels in
a woman who is not pregnant or breast feeding reduces lipid (fat) metabolism. Over 30 000
Swedish men and women may have raised levels of prolactin. Women who are pregnant or
breast feeding have naturally raised levels of prolactin, but stress, some medicines and
benign brain tumours can also lead to raised levels of the hormone. In many cases doctors
dont know what causes the rise in hormone levels. In women, an abnormally high level
can cause menstrual disturbances and infertility, and may also result in insulin
resistance. In recent years scientists have also recognised the role of prolactin in
the development of obesity, but little research has been done into the precise mechanism
by which prolactin regulates metabolism, says Louise Nilsson. In her thesis Louise
Nilsson shows that there are receptors for the breast feeding hormone in human fatty
tissue.

New evidence that genetics plays a key role in obesity is published today in the
International Journal of Bioinformatics Research and Applications. The findings relate to
the genetics of modern Pima Indians who have an unusually high rate of obesity but could
be extrapolated to all people. Their obesity is thought to be linked to a thrifty
metabolism that allowed them to metabolize food more efficiently in times when little was
available but causes problems when food is in abundance.

Is there a prospective association
between obesity and periodontal disease?

This is the question asked by a team of investigators from the Harvard School of Public
Health and the University of Puerto Rico, reporting their findings today during the 87th
General Session of the International Association for Dental Research, convening at the
Miami Beach Convention Center. The investigators evaluated the association between
different measures of obesity and risk of periodontal disease. They analyzed data from
36,903 men from the Health Professionals Follow-Up Study who were free of reported
periodontal disease at the start of follow-up, and we followed them for up to 16 years
(1986-2002). Height was assessed at the start of follow-up, and weight and self-reported
periodontal disease data were collected at baseline and on follow-up questionnaires mailed
every two years. Measures of central obesity were made by waist and hip circumference
through self-assessed measurements and reported in 1987 with the aid of printed
instructions and a tape measure. Self-reported periodontal disease and adiposity measures
had been previously validated. They evaluated the effect of body mass index (BMI kg/m2),
waist circumference (WC), and waist-to-hip ratio (WHR), on first report of periodontal
disease diagnosis. The team observed significant associations between all measures of
obesity and periodontal disease when accounting for age, smoking, race, dental profession,
physical activity, fruit and vegetable intake, and diabetes status at baseline. Obesity
(BMI > 30 kg/m¨2) at the beginning of follow-up and over follow-up was significantly
associated with a 25% and 29% increased risk compared with normal weight (BMI 18.5-24.9
kg/m2), respectively. Men with WC > = 40 inches compared with <40 inches was significantly associated with a 19% increased risk of periodontal disease, compared with men with a WC < 40 inches. WHR> = 0.95 compared with <0.95 exhibited a significant 16% increased risk of periodontal disease. When BMI was accounted for (i.e., overall obesity), the effects of WC and WHR (i.e., central obesity) were weakened. The associations of BMI and WC were significant even among non-diabetics and among those who had never smoked. These results provide the first evidence following a large group of people over time with clear evidence of obesity occurring prior to periodontal disease, and support an association between obesity and risk of periodontal disease. Given the high prevalence of obesity and periodontal disease, this association may be of substantial public health importance.

Fat-derived inflammatory factor may
explain diseases that come with obesity

An inflammatory factor already linked to several diseases, including pulmonary disease,
lung cancer, and arthritis, may also be responsible for the insulin resistance that comes
with obesity, according to a new study published in the April issue of Cell Metabolism, a
Cell Press publication. Researchers have found that the inflammatory chemokine known as
CXCL5 rises and falls with obesity and subsequent weight loss in humans. (Chemokines are
structurally related signaling proteins that are secreted by cells.) They found further
evidence tying the inflammatory factor, which is produced and secreted at high levels by
fat tissue, to insulin resistance in mice. What's more, they show that treatments designed
to block its action improves the animals' sensitivity to insulin. "Clearly, this
finding could be a big development for understanding the side effects of obesity,"
said Lluis Fajas of INSERM in France. "It offers a new target for therapy and new
hope for subjects to improve their pathology." Fat tissue known as white adipose
tissue (WAT) is primarily involved in energy storage in the form of triglycerides and
energy release in the form of free fatty acids, Fajas' team explained. However, WAT is
more than a fat storage organ; it also secretes numerous other factors with roles in both
health and disease. In the new study, the researchers show that CXCL5 is one of those
factors. The chemokine is expressed at high levels in WAT, particularly in immune cells
known as macrophages. Moreover, they report that CXCL5 is dramatically increased in the
blood of people who are obese compared to those who are lean. Those CXCL5 levels drop when
obese people lose weight and are also lower in obese individuals that continue to respond
to insulin than in those who are insulin resistant. They further found that treatment with
recombinant CXCL5 blocks insulin-stimulated glucose uptake in the muscles of mice. What's
more, treatment of obese, insulin-resistant mice with either anti-CXCL5 neutralizing
antibodies or drugs that block the receptor it triggers (known as CXCR2) reverses those
symptoms. Mice lacking the CXCL5 receptor are also protected against obesity-induced
insulin resistance. Overall, the findings show that CXCL5 produced by fat tissue
"represents a link between obesity, inflammation, and insulin resistance."
Interestingly, they added, the CXCR2 receptor is active outside of muscle, in cells that
line blood vessel walls and in the lung and intestine, for example. Therefore, increased
CXCL5 circulating levels as observed in obesity could lead to other problems, including
atherosclerosis and other inflammatory diseases."Studies aiming to elucidate the role
of WAT-secreted CXCL5 in all these obesity-related pathologies are likely to be
forthcoming in the near future," they wrote. "Inhibiting CXCL5 secretion or
function in obese individuals may not only ameliorate their insulin sensitivity, but could
also decrease the risk of developing other major obesity-related pathologies."

For Overweight Patients With
Insulin Sensitivity, Even One Session Of Exercise Can Improve Metabolic Health

One out of every three Americans is obese. These individuals are at greater risk for
additional diseases, since obesity leads to other health problems, such as diabetes.
Obesity-related complications are associated with an abnormal fat metabolism in the
muscle. As a result, accumulated fat by-products inside the muscle affect insulin
resistance. To avoid the build up of fat by-products, fat must either be oxidized (burned,
as in exercise) or stored (as benign fat) in muscle. A team of researchers has examined
the effect of exercise on fat accumulation in a new study involving five obese women. In
one session the women overate and did not exercise; in a follow-on session they overate
and did exercise.

Its a small study about how eating a certain type of breakfast can help you burn
more fat, but it could nonetheless have a huge impact on losing unwanted pounds or
maintaining a healthy weight. British researchers have determined that high-fiber,
low-glycemic foods are best for kick-starting your weight-loss program.

A research study to be presented at the 2007 Annual Scientific Meeting of The Obesity
Society, found that chewing gum before an afternoon snack helped reduce hunger, diminish
cravings and promote fullness among individuals who limit their overall calorie intake.
Calorie intake from snacks was significantly reduced by 25 calories. Overall, this study
demonstrates clearly the benefits of chewing gum and highlights the potential role of
chewing gum in appetite control and weight management.

Experts don't dispute the important role that diet and activity play in maintaining a
healthy weight. But can poor eating habits and a less active lifestyle fully explain the
prevalence of obesity in the US today? That question has led some researchers to ask
whether there might be other causes for this serious problem.

Add one more label to the list consumers are increasingly being asked to parse - This one
declares food items as "low glycemic," and refers to a food's effects on blood
sugar levels. Low-glycemic diets have become popular in England and Australia, based on
studies that suggest they could help manage diabetes and prevent heart disease and
obesity, and they're now making headway here in the U.S.

According to a new book by former FDA chief Dr. David Kessler, many neuroscientists
believe that certain people have an addiction to harmful foods, much like those who are
addicted to alcohol or drugs.

Weight loss with vegetable juice is achieved in a number of other ways, including boosting
your energy levels to make you more active overall, as well as balancing the acids that
are stored in fat cells. When your body is more energized, it can burn off more calories.

In recent years, obesity has taken on epidemic proportions in developed nations,
contributing significantly to major medical problems, early death and rising health care
costs. According to Centers for Disease Control and Prevention estimates, at least a
quarter of all American adults and more than 15 percent of children and adolescents are
obese.While recent research advances and treatment methods have had little effect in
reducing obesity levels, researchers at the UCLA Henry Samueli School of Engineering and
Applied Science, in collaboration with the David Geffen School of Medicine at UCLA, may
have discovered a completely new way to approach the problem. In a study to be published
in the June 3 issue of the journal Cell Metabolism, chemical and biomolecular engineering
professor James Liao, associate professor of human genetics and pediatrics Katrina Dipple
and their research team demonstrate how they successfully constructed a non-native pathway
in mice that increased fatty acid metabolism and resulted in resistance to diet-induced
obesity. "When we looked at the fatty-acid metabolism issue, we noted there are two
aspects of the problem that needed to be addressed," Liao said. "One is the
regulation; fatty acid metabolism is highly regulated. The other is digestion of the fatty
acid; there needs to be a channel to burn this fat." "We came up with an
unconventional idea which we borrowed from plants and bacteria," said Jason Dean, a
graduate student on Liao's team and an author of the study. "We know plants and
bacteria digest fats differently from humans, from mammals. Plant seeds usually store a
lot of fat. When they germinate, they convert the fat to sugar to grow. The reason they
can digest fat this way is because they have a set of enzymes that's uniquely present in
plants and bacteria. These enzymes are called the 'glyoxylate shunt' and are missing in
mammals." To investigate the effects of the glyoxylate shunt on fatty acid metabolism
in mammals, Liao's team cloned bacteria genes from Escherichia coli that would enable the
shunt, then introduced the cloned E. coli genes into the mitochondria of liver cells in
mice; mitochondria are where fatty acids are burned in cells.

Researchers have found a clue about how resistance to the hormone leptin might disrupt the
brain signals that tell the body when to stop eating. The research, which focused on the
rare genetic disorder Bardet-Biedl syndrome, also found an association between leptin
resistance and high blood pressure. The findings, which were based on mouse models, have
implications for treating BBS as well as obesity and high blood pressure in people without
BBS.

Researchers have uncovered new evidence suggesting factors other than genes could cause
obesity, finding that genetically identical cells store widely differing amounts of fat
depending on subtle variations in how cells process insulin. Learning the precise
mechanism responsible for fat storage in cells could lead to methods for controlling
obesity. "Insights from our study also will be important for understanding the
precise roles of insulin in obesity or Type II diabetes, and to the design of effective
intervention strategies," said Ji-Xin Cheng, an assistant professor in Purdue
University's Weldon School of Biomedical Engineering and Department of Chemistry.

Two cell proteins that relax the gut and help accommodate a big meal have been identified
by UCL scientists. The proteins could offer a future drug target against weight gain, by
preventing the stomach from expanding.

Cold and brown fat raise the
prospect of a new method of treating obesity

Sven Enerbšck, Professor at the Institute of Biomedicine at the Sahlgrenska Academy,
University of Gothenburg, Sweden, is one of the scientists who published their results in
The New England Journal of Medicine this week. Studies carried out by Enerbšck and others
show that adults use brown fat to convert energy to heat - a discovery that may provide
new possibilities in treating overweight and obesity. It has previously been believed that
the brown fat found in infants disappears as we grow up, but the new study shows that this
is not the case. Brown fat cells have been found in adults, in the lower part of the neck
just above the collarbone.

The spiralling increase in obesity rates in the Western and developing worlds has brought
with it a host of related metabolic complications including diabetes, dyslipidaemia,
cardiovascular complications, and cancer. Whereas obesity itself presents its own
independent health problemssuch as sleep apnoea or psychological issuesthe
vast majority of obesity-related mortality is caused by these secondary metabolic
complications. The link between obesity and such complications as insulin resistance is
well established on a population level but poorly understood mechanistically. Efforts to
tackle the obesity epidemic through public health initiatives and drugs have so far been
notable for their lack of success. With little prospect for halting the obesity epidemic,
treatment of its associated diseases becomes of paramount importance both for public
health and associated costs.

University of Cincinnati pathologists have identified a new molecular target that one day
may help scientists develop drugs to reduce fat transport to adipocytes in the body and
prevent obesity and related disorders, like diabetes.

By inserting a molecular shunt into the livers of mice, researchers have shown they can
make the animals burn more fat. That so-called glycoxylate shunt consists of two metabolic
enzymes normally found in bacteria and plants, but not in mammals, according to the report
in the June issue of Cell Metabolism, a Cell Press publication. "It's an additional
channel for burning fat to control obesity," said James Liao of the University of
California, Los Angeles. "This creates a shortcut through [the normal pathway],"
added Katrina Dipple, also of UCLA. "It's like putting in a toll road." In the
beginning, the researchers really didn't know what to expect the enzymes taken from E.
coli bacteria would do when placed in mammalian cells. In fact, the glycoxylate shunt
actually prevents the complete oxidation of fat in the organisms in which it is normally
found. "There was no guarantee it would work," Liao said. "But we were
brave enough to try." Remarkably, they found that human liver cells expressing the
enzymes burn more fat. Likewise, mice with the shunt resist becoming obese despite eating
a high-fat diet.

Mice lacking the fat hormone leptin or the ability to respond to it become morbidly obese
and severely diabeticnot to mention downright sluggish. Now, a new study in the June
Cell Metabolism shows that blood sugar control in those animals can be completely restored
by returning leptin sensitivity to a single class of neurons in the brain, which account
for only a small fraction of those that normally carry the hormone receptors. "Just
the receptors in this little group of neurons are sufficient to do the job," said
Christian Bjorbaek of Harvard Medical School. What's more, animals with leptin receptors
only in the so-called pro-opiomelanocortin (POMC) neurons spontaneously increase their
physical activity levels despite the fact that they remain profoundly obese. While
understanding exactly how the POMC neurons act on other organs remains a future challenge,
the discovery suggests that drugs designed to tap into the pathwayturning up or down
the dial, so to speakmight have benefit for those with severe diabetes and obesity,
according to the researchers. Such drugs might even encourage obese individuals to get
moving. "This gives us the opportunity to search for drugs that might induce the
desire or will to voluntarily exercise," Bjorbaek said. Leptin was first identified
15 years ago and made famous for its ability to curb appetite and lead to weight loss. It
is known to play a pivotal role in energy balance through its effects on the central
nervous system, specifically by acting on a hypothalamic brain region known as the arcuate
nucleus (ARC). The ARC contains two types of leptin-responsive neurons, the POMC neurons,
which cause a loss of appetite, and the so-called Agouti-related peptide (AgRP) neurons,
which do the opposite. Studies had also revealed a role for leptin in blood sugar control
and activity level, also via effects on the ARC. However, scientists still didn't know
which neurons were responsible, until now.

The researchers defined "normal weight" by body mass index. They found that
people with normal BMI who had the highest percentage of body fat were also those who had
metabolic disturbances linked to heart disease.

Mice with increased levels of a natural brain chemical don't gain weight when fed a
high-fat diet, researchers at UT Southwestern Medical Center have found.The chemical,
orexin, works by increasing the body's sensitivity to the "weight-loss hormone,"
leptin, the researchers report. Finding a way to boost the orexin system may prove useful
as a therapy against obesity, said Dr. Masashi Yanagisawa, professor of molecular genetics
at UT Southwestern and senior author of the study, which appears in the January issue of
Cell Metabolism. "Obese people are not deficient in leptin," Dr. Yanagisawa
said. "They have tons of leptin floating around. The problem is that their brain
isn't very sensitive to it." Orexin, which Dr. Yanagisawa discovered about a decade
ago, is involved in controlling appetite and sleep. He found that reduced levels of orexin
lead to the sleep disorder narcolepsy in both rodents and humans. Orexin can boost the
appetite in the short term, but, paradoxically, a lack of orexin leads to obesity in the
long run. "It's been confusing," said Dr. Yanagisawa, an investigator with the
Howard Hughes Medical Institute at UT Southwestern. Part of the confusion comes about
because orexin acts on two different molecules in the brain, OX1R and OX2R. In the current
study, the researchers aimed to distinguish which action was involved in weight control.
The researchers increased the levels of orexin in mice, either through genetic engineering
or by administering the hormone into the brain.

If identical twins eat and exercise equally, must they have the same body weight? By
analyzing the fundamental equations of body weight change, NIH investigators Carson Chow
and Kevin Hall find that identical twins with identical lifestyles can have different body
weights and different amounts of body fat.

Researchers at UT Southwestern Medical Center have found that a single gene might control
whether or not individuals tend to pile on fat, a discovery that may point to new ways to
fight obesity and diabetes.

A new study in the September issue of Cell Metabolism, a publication of Cell Press, points
to a new method for burning off all those irresistible extra caloriesby turning on
an energy-draining, but otherwise futile, cycle of protein synthesis and breakdown.
Christopher Lynch of The Pennsylvania State University College of Medicine and his
colleagues found that they could drive such heightened protein turnover in mice by
disrupting an enzyme involved in the metabolism of some amino acids, the building blocks
of proteins. The enzyme-deficient animals showed elevated blood levels of the essential
amino acid leucine, an important nutrient signal, and became slimmer than normal mice
despite eating more food. They also showed remarkable improvements in glucose
and insulin tolerance, and resistance to becoming obese on a high-fat diet. The mice
on the outside look normal, just skinnier and smaller, Lynch said. After
looking at their metabolism, we found that for the same activity, they were using more
energy. Moreover, the researchers found that the animals that ate the most food also
expended the most energy. That would be ideal for people who are overweight,
Lynch said. They could continue to eat and just waste the energy and be thin.

A study conducted by researchers at Mayo Clinic shows that obese patients with specific
genetic makeup had enhanced response to the weight loss drug sibutramine, while others who
lack these genetic factors lost little or no weight.The findings are published in the
October issue of Gastroenterology. In this randomized, double-blind, placebo-controlled
study, Mayo researchers measured the impact of two different dosage levels of sibutramine
(10 or 15 mg daily) combined with behavioral therapy for 12 weeks in 181 overweight or
obese participants. Participants received structured behavioral therapy for weight
management at four, eight and 12 weeks.As has been previously shown in trials with this
approved medication, patients who received sibutramine and behavioral therapy lost
significantly more weight than those who received placebo and the same behavioral therapy.
Researchers also confirmed that weight loss at four weeks was a significant predictor of
weight at 12 weeks, even after adjusting for baseline weight, gender, BMI and
treatment.Researchers explored the influence on weight and body composition of specific
genetic markers indicative of variation in the function of two hormones/transmitters and
an intracellular protein that mediates the function of those hormones. Patients with a
certain pattern of variations of the genes lost an average of 10-12 pounds over the
12-week study, and those with unfavorable variations did worse.

Breakfast choices impact hunger and
calorie consumption throughout day

New studies presented this week at Experimental Biology 2009 enhance the growing body of
evidence supporting the nutritional benefits of eggs. Research presented at the meeting
demonstrates that choosing eggs for breakfast can help adults manage hunger while reducing
calorie consumption throughout the day. Additional research shows that teens who choose a
protein-rich breakfast are less hungry and eat fewer calories at lunch.

Mice whose fat cells were allowed to grow larger than fat cells in normal mice developed
healthy obesity when fed a high-fat diet, researchers at UT Southwestern
Medical Center found in a new study. The fat but healthy mice lacked a protein called
collagen VI, which normally surrounds fat cells and limits how large they can grow, like a
cage around a water balloon. The findings appear online and in a future edition of
Molecular and Cellular Biology. The mice lacking collagen VI fared much better
metabolically than their counterparts that retained this particular collagen, said
Dr. Philipp Scherer, director of the Touchstone Center for Diabetes Research at UT
Southwestern and the studys senior author. The mice without collagen VI
dont develop inflammation or insulin resistance. They still get obese, but its
a healthy obesity. When people take in more calories than needed, excess
calories are stored in adipose or fatty tissue. The fat cells are embedded in and secrete
substances into an extracellular matrix, a type of connective tissue that provides support
to fat tissue, like scaffolding. Collagen VI is one component of the extracellular matrix.
Too much of this connective tissue prevents individual cells from expanding and can lead
to fibrosis and eventually inflammation.

Theres no doubt about it, people all over the world are getting fatter. Could a
virus be to blame, asks Bob Holmes? WHAT IF YOU COULD CATCH OBESITY as easily as you can
catch a cold? Just one unlucky sneeze in a crowded railway carriage or lift, and
thats it. Bang! Never mind that youve been a string bean all your life. Never
mind that youve always taken plenty of exercise and watched what you eat. Pick up
the wrong virus, and youre almost certain to get fat. It sounds preposterous, but
remember that only a few years ago the idea that a bacterium could give you ulcers or
heart disease sounded crazy. Those theories are now well acceptedand the
obesity virus could be the next one to become respectable. Traces of the virus
show up in enough overweight people to suggest that the epidemic of obesity in
todays world may be more than a mere metaphor. But dont sidle away from that
extra-large person on the train just yet. Your greatest risk of catching obesity might
come from someone you least expect.

Charles Darwin and his contemporaries postulated that food consumption in birds and
mammals was limited by resource levels, that is, animals would eat as much as they could
while food was plentiful and produce as many offspring as this would allow them to.
However, recent research has shown that, even when food is abundant, energy intake reaches
a limit, even in animals with high nutrient demands, such as lactating females. Scientists
at the Research Institute of Wildlife Ecology in Vienna suggest that this is due to active
control of maternal investment in offspring in order to maintain long-term reproductive
fitness. The research, to be presented by Dr Teresa Valencak at the Society for
Experimental Biology Annual Meeting in Glasgow has shown that, when their energy reserves
are low or when their offspring are kept in cooler temperatures, Brown hares are able to
increase their energy turnover and rate of milk production above that normally observed.
This indicates that, ordinarily, the hares are operating at below their maximum capacity
and shows that this is not due to any kind of physiological constraint, such as length of
digestive tract or maximum capacity of mammary glands. Also, as the hares were provided
with plentiful food, there could be no limitation of energy turnover due to food
availability. The way that females regulated their energy expenditure according to pup
demand and their own fat reserves but did not exceed certain levels fitted with the
group's theory that using energy at close to the maximum rate has costs for animals which
may compromise their ability to successfully reproduce in the future. If a hare puts most
of its energy into a litter of pups then it will have little left over for growth and body
repairs for example, which may shorten its life or make it less able to produce or care
for young in the future. By actively limiting the rate of energy turnover, a mother can
prevent this and maintain a higher level of reproductive success over her lifetime.

In a discovery that counters prevailing thought, a study in mice has found that
inactivating a pair of key genes involved in "fat-burning" can actually increase
energy expenditure and help lower diet-induced obesity. These unusual findings, appearing
this week in the JBC, might lead to some new roads in weight-loss therapy. Humans and
other warm-blooded animals need to continually "burn fat" in order to maintain
body temperature, and it's currently believed that an individual's fat-burning capacity,
or thermogenic potential, is connected with obesity risk; that is, people with more
thermogenic potential are less likely to become obese. In fact, bodybuilders and dieters
looking to burn fat commonly use thermogenic supplements like ephedra. In theory, lowering
thermogenesis should increase the chances of obesity, but Leslie Kozak and colleagues at
Pennington Biomedical Research Center found that this may not be the case. They
knocked-out two thermogenic genes in mice, Ucp1 (mitochondrial uncoupling protein) and Gdm
(glycerol 3-phosphate dehydrogenase) and then fed the mice a high-fat diet while rearing
them at a cool 20 įC (68 įF). Surprisingly, these mice were actually quite resistant to
obesity, which resulted from the mice turning on backup heat generators, so to speak.
Lacking Ucp1 and Gdm, genes that have been designed for the efficient production of heat,
mouse white fat cells activated alternate, and more inefficient, fat burning pathways. In
this case, though, inefficiency is beneficial, as the mice had to burn more fat than
normal to stay warm (by analogy you burn more wood by warming your house with an open fire
then with a well designed wood stove). Importantly, after spending 10 weeks at 20 įC the
mice retained these alternate pathways even after transferring to 28 įC (82 įF),
suggesting their bodies had adapted to the change. Thus, Kozak and colleagues note, fat
burning does not necessarily require making thermogenesis easier; by making it harder and
forcing the body to use inefficient methods to stay warm, the same goals can be reached.

Mayo Clinic Proceedings examines
link between bacteria in the digestive system and obesity

According to John DiBaise, M.D., a Mayo Clinic Arizona gastroenterologist and lead author
of the Mayo Clinic Proceedings article, several animal studies suggest that gut microbiota
are involved in regulating weight, and that modifying these bacteria could one day be a
treatment option for obesity.

Common virus may contribute to
obesity in some people, new study shows

A common virus may cause obesity in some people, according to new evidence in a controlled
laboratory study. Scientists showed that infection with human adenovirus-36 (Ad-36), long
recognized as a cause of respiratory and eye infections in humans, transforms adult stem
cells obtained from fat tissue into fat cells. The study, which might lead to new
treatments for obesity, will be reported in August at the American Chemical Society
national meeting in Boston.

How much we want to eat, in other words our appetite, and how much energy we burn, are
both controlled by a hormone known as leptin. Leptin is made by fat tissue and it passes
through the circulation to the brain, where it modifies the activity of several types of
nerve cell, including POMC nerves, to signal to the body that it does not need to eat more
and that it needs to burn more energy. As obesity can be caused if leptin-mediated
signaling goes awry, much effort is being expended trying to identify the signaling
pathways activated by leptin. Joel Elmquist and colleagues, at the University of Texas
Southwestern Medical Center, Dallas, have provided new insight into the signaling pathways
by which leptin mediates its effects on POMC nerves in mice.

Have you ever wondered why some healthy-looking people drop dead from a heart attack after
exercise? Its never when they are exercising; it is when they stop and rest.
Its not the exercise that killed them; its the poor recovery time. Exercise is
stress to the body and a healthy body is supposed to adapt to stress and rebound or bounce
back.

A chocolate cookie a day puts 20
pounds on an energetically-balanced kid in 4 years

So-called "miracle diets," such as the South Beach diet, the Atkins diet or the
Artichoke diet, lack scientific foundations and are a danger for health. Specialists'
recommendations include a daily 500 to 700 calorie deficit, depending on body weight, age
and physical exercise, as well as a high-fiber diet to gradually lose 6.5 pounds a month.

To understand where fat comes from, you have to start with a skinny mouse. By using such a
creature and observing the growth of fat after injections of different kinds of immature
cells, Rockefeller Fat chance. Using an animal strain called the leptin-luciferase mouse,
Rockefeller University researchers observed the formation of fat from precursor cells over
12 weeks. A luminescent marker (red) switches on to indicate where mature fat cells have
developed. University scientists have discovered an important fat precursor cell that may
in time explain how changes in the numbers of fat cells might increase and lead to
obesity. The finding, published online in this weeks issue of the journal Cell,
could also have implications for understanding how fat cells affect conditions such as
diabetes and cardiovascular disease.

Researchers studying the enzyme that converts starch to simple sugars like glucose have
found that people living in countries with a high-starch diet produce considerably more of
the enzyme than people who eat a low-starch diet.

New research led by the University of Cincinnati (UC) suggests that the hunger hormone
ghrelin is activated by fats from the foods we eatnot those made in the bodyin
order to optimize nutrient metabolism and promote the storage of body fat. The findings,
the study's author says, turn the current model about ghrelin on its head and point to a
novel stomach enzyme (GOAT) responsible for the ghrelin activation process that could be
targeted in future treatments for metabolic diseases. The laboratory study, led by
Matthias TschŲp, MD, UC associate professor of psychiatry and internal medicine, is
published online ahead of print Friday, June 5, 2009, in the journal Nature Medicine.
Ghrelin is a hormone that was believed to accumulate during periods of fasting and is
found in the body in high concentrations just before meals. It is dubbed the "hunger
hormone" because it has been shown that administration of pharmacological doses acts
in the brain to stimulate hunger and increase food intake in animal models and humans. The
ghrelin hormone is unique in that it requires acylation (the addition of a fatty acid) by
a specific enzyme (ghrelin O-acyl transferase, or GOAT) for activation. Originally it was
assumed that the fatty acids attached to ghrelin by GOAT were produced by the body during
fasting.The new data by TschŲp and his team suggests that the fatty acids needed for
ghrelin activation actually come directly from ingested dietary fats. In a departure from
an earlier model that was upheld for nearly a decade, TschŲp says, it appears that the
ghrelin system is a lipid sensor in the stomach that informs the brain when calories are
availablegiving the green light to other calorie-consuming processes such as
growing. TschŲp and his team used mouse models to test the effects of over expressing the
GOAT enzyme, or "knocking it out." They found that, when exposed to a lipid-rich
diet, mice without GOAT accumulated less fat than normal mice, while those with
over-expressed GOAT accumulated more fat mass than normal mice. "When exposed to
certain fatty foods, mice with more GOAT gain more fat," says TschŲp. "Mice
without GOAT gain less fat since their brain does not receive the 'fats are here, store
them' signal."

In investigating the complex neurocircuitry behind weight gain and glucose control,
scientists have known that the hormone leptin plays a key role in the process. But within
the myriad twists and turns of the brains intricate landscape, the exact pathways
that the hormone travels to exert its influence have remained a mystery.Now, a study led
by Harvard investigators at Beth Israel Deaconess Medical Center (BIDMC) sheds further
light on the subject. Reported in the journal Cell Metabolism, the findings demonstrate
that when leptin sensitivity is restored to a tiny area of neurons in the brains
hypothalamus, a group of mice deficient in the leptin receptor are cured of severe
diabetes  and also spontaneously double their activity levels  independent of
any change in weight or eating habits.

A Texas AgriLife Research scientist and fellow researchers have discovered that arginine,
an amino acid, reduces fat mass in diet-induced obese rats and could help fight human
obesity. "Given the current epidemic of obesity in the U.S. and worldwide, our
finding is very important, said Dr. Guoyao Wu, an AgriLife Research animal
nutritionist in College Station and Senior Faculty Fellow in the department of animal
science at Texas A&M University. The research found dietary arginine supplementation
shifts nutrient partitioning to promote skeletal-muscle gain, according to the
researchers. The findings were published recently in the Journal of Nutrition
(http://jn.nutrition.org). In laboratory experiments, rats were fed both low-and high-fat
diets. They found that arginine supplementation for a 12-week period decreased the body
fat gains of low-fat and high-fat fed rats by 65 percent and 63 percent, respectively. The
long-term arginine treatment did not have any adverse effects on either group. This
finding could be directly translated into fighting human obesity, Wu said. At
this time, arginine has not been incorporated into our food (but could in the
future).

Scientists at the University of North Carolina at Chapel Hill School of Medicine have
discovered a gene that when mutated causes obesity by dampening the body's ability to burn
energy while leaving appetite unaffected. The new research could potentially lead to new
pharmacologic approaches to treating obesity in humans that do not target the brain,
according to study senior author Yi Zhang, Ph.D., Howard Hughes Medical Institute
investigator and professor of biochemistry and biophysics in the UNC School of Medicine.
Zhang is also a member of the UNC Lineberger Comprehensive Cancer Center. The findings
also add new knowledge to the burgeoning field of epigenetics, in which heritable changes
in gene expression or physical appearance are caused by mechanisms besides changes in the
underlying DNA. The gene in question encodes for a specific epigenetic factor, an enzyme
called Jhdm2a. In 2006, Zhang showed that Jhdm2a was able to demethylate, or remove, a
methyl group from one of four histone proteins bound to all genes. Because they are so
intimately associated with DNA, even slight chemical alterations of histones can have
profound effects on nearby genes. The new study focused on a line of so-called
"knockout" mice that lacked the Jhdm2a gene. Zhang found impairment in two
molecular signaling pathways important for normal function in brown fat tissue and muscle
cells. Both pathways exert a major influence on metabolism, the body's conversion of food
to energy. Without the enzyme, the mice had reduced metabolisms, becoming visibly obese.
To Zhang's knowledge, this is the first mouse model to exhibit obese traits that do not
resulting from an alteration in appetite, which is largely a brain function. "Given
that this gene is not expressed in the brain, any drug that targets this gene would not
have an effect on brain function," he said. "Therefore, we are really looking
for a pure effect on metabolism."

An interesting discovery was published in the Sept. 14 issue of the World Journal of
Gastroenterology. A research group led by Dr. Corazziari from the University La Sapienza°
of Rome discovered that gastro-esophageal reflux disease (GERD) is more popular with
overweight women than within the average population. Meanwhile, there is no correlation
between GERD and being overweight in men. Dr. Corazziari suggested that higher oestrogen
concentration, which is common in overweight females, is an important factor in causing
GERD

As body mass increases, so does a patients risk of urinary tract infection (UTI),
according to Baltimore researchers. A new study, presented at the 104th Annual Scientific
Meeting of the American Urological Association (AUA) assesses and stratifies this risk.
Researchers evaluated insurance claims of 95,962 subjects over a five year period (from
2002 through 2006) to identify whether obesity is associated with a UTI diagnosis. The
results show that, as BMI increased, the odds of being diagnosed with a UTI increased as
well. This association was strongest for morbidly obese patients. The effect of the
obesity epidemic in the United States transcends any one medical specialty or
condition, said Anthony Y. Smith, MD, an AUA spokesman. Patients with elevated
body mass index should be vigilant about urologic health because even the most simple of
urinary tract infections can be deadly if left untreated.

Researchers at Georgia State University have found that fat cells give feedback to the
brain in order to regulate fat burning much the same way a thermostat regulates
temperature inside a house. With an increase in obesity threatening the health and life
expectancies of people across the world, the research may help scientists better
understand how weight is shed. C. Kay Song and Tim Bartness of Georgia State, along with
Gary J. Schwartz of the Albert Einstein College of Medicine, found that during the process
of burning fat  called lipolysis  fat cells use sensory nerves to feed
information to the brain. Using viruses to trace communications in the nerves of Siberian
hamsters, they found that the brain uses part of the nervous system used to regulate body
functions, called the sympathetic nervous system, to in turn communicate back to the cells
to initiate, continue or stop the fat burning depending upon the information the brain
receives from the fat. "The brain can trigger lipid burning by fat cells and through
these sensory nerves, the fat cell can give the brain feedback," Bartness explained.
"This is a really important concept in biology, as it can regulate the process of
lipolysis much like how a thermostat regulates temperature in your house, using input from
the air and output to a furnace or heating unit. "The presence and function of the
sensory nerves has been completely ignored and the areas in the brain that receive this
sensory information were unknown until we did these studies," he said. When the body
has a low amount of a type of readily available fuel, a carbohydrate called glycogen, the
body starts lipolysis to release energy stored in fats. At the end nerves which are part
of the sympathetic nervous system, a chemical called norepinephrine is released to trigger
the breakdown of fat.

You see the commercials television and advertisements in magazines touting the benefits of
the newest weight loss tool or diet on the market. But dont get carried away with
your credit card. You can forget spending tons of money on expensive exercise machines or
fad diets. A new research study shows that by using this simple tool you can dramatically
increase your weight loss success. And it doesnt cost a fortune! Keep reading to
find out about this simple, inexpensive investment into your weight loss efforts.

Scientists at the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ)
have discovered a mechanism in liver metabolism that is responsible for pathologically
elevated blood fat levels found in severe metabolic disorders. Mice suffering from
metabolic syndrome or type 2 diabetes produce only small amounts of a molecule called LSR
in the liver, as reported by researchers headed by Dr. Stephan Herzig of DKFZ in the
specialist journal Diabetes. As a result, only small amounts of fat are transported from
the blood into the liver and blood fat levels rise immensely. Stephan Herzig heads the
Research Group "Molecular Metabolic Control" at DKFZ.

Enjoying the eating process without focus on dietary restrictions may be key to managing
weight and staying healthy, according to researchers who have unveiled a new and effective
model for managing eating.

Greater maternal body mass index during offspring development does not have a marked
effect on offspring fat mass at ages nine to eleven years, according to a new study from
the University of Bristol published today in PLoS Medicine.

Being overweight is a health concern, and using only body mass index (BMI) to determine
weight classification may not give an accurate picture of a persons health,
according to an advisory published in Circulation: Journal of the American Heart
Association. About one-third of the U.S. population is overweight  the middle range
between normal weight and obesity. Overweight in adults is a BMI of 25.0 to 29.9. BMI is a
numerical value of weight in relation to height. Studies that examined the relationship
between overweight (as measured by BMI) and risk of death from all causes (often referred
to as total mortality) have had contradictory results. However, considering death from all
causes overlooks the role that overweight may play in the development of risk factors for
cardiovascular diseases. Even among the young, overweight is related to the development of
serious risk factors for cardiovascular disease, such as high blood pressure, obesity,
elevated levels of cholesterol and type 2 diabetes.

Overweight individuals who ate a low-calorie, low-carbohydrate diet high in plant-based
proteins for four weeks lost weight and experienced improvements in blood cholesterol
levels and other heart disease risk factors, according to a report in the June 8 issue of
Archives of Internal Medicine, one of the JAMA/Archives journals. A high-carbohydrate,
low-fat vegetarian diet also resulted in weight loss but without the additional
cardiovascular benefits. "There is a dilemma relating to the proportion and source of
fat, protein and carbohydrate that constitutes the optimal weight loss and
cholesterol-lowering diet," the authors write as background information in the
article. Newer dietary approaches for the prevention and treatment of chronic disease
emphasize increased fruit and vegetable intake and reduced meat consumption. However,
low-carbohydrate diets with increased meat consumption have also been promoted for body
weight reduction and the prevention and treatment of diabetes and coronary heart disease.
These diets have been shown to be effective in inducing weight loss, reducing insulin
resistance, lowering blood fats known as triglycerides and raising high-density
lipoprotein cholesterol (HDL-C, or "good" cholesterol) levels, but have tended
to increase low-density lipoprotein cholesterol (LDL-C, or "bad" cholesterol)
levels. "This lack of a benefit for LDL-C control is a major disadvantage in using
this dietary strategy in those already at increased risk of coronary heart disease,"
the authors write. David J.A. Jenkins, M.D., of St. Michael's Hospital and the University
of Toronto, Ontario, Canada, and colleagues tested the effects of a low-carbohydrate diet
high in vegetable proteins from gluten, soy, nuts, fruits, vegetables, cereals and
vegetable oils among overweight men and women with high LDL cholesterol levels. A total of
25 participants were randomly assigned to consume this dietthe
"Eco-Atkins" dietfor four weeks, while an additional 25 participants ate a
control diet that was high-carbohydrate, lacto-ovo vegetarian and based on low-fat dairy
and whole grain products. Study food was provided to participants at 60 percent of their
estimated calorie requirements. Of the 47 participants who began the study, 44 (22 in each
group) completed the four-week period. Weight loss was similarabout 4 kilograms or
8.8 poundsin both groups. However, reductions in LDL-C levels and improvements in
the ratios between total cholesterol and HDL-C were greater for the low-carbohydrate diet
compared with the high-carbohydrate diet. The low-carbohydrate diet also appeared to
produce beneficial changes in levels and ratios of apolipoproteins, proteins that bind to
fats. In addition, small but significantly greater reductions were seen in both systolic
(top number) and diastolic (bottom number) blood pressure for the low-carbohydrate vs. the
high-carbohydrate group.Pending answers to important questions, including whether further
reducing carbohydrate intake would produce additional benefits, "a plant-based
low-carbohydrate diet high in vegetable proteins and oils may be an effective option in
treating those with dyslipidemia for whom both weight loss and lower LDL-C concentrations
are treatment goals," the authors conclude.

Obesity very often leads to insulin resistance, and now researchers reporting in the July
8 issue of Cell Metabolism, a Cell Press publication, have uncovered another factor behind
that ill consequence. The newly discovered culprita protein known as pigment
epithelium-derived factor (PEDF for short)is secreted by fat cells. They also report
evidence to suggest that specifically blocking that protein's action may reverse some of
the health complications that come with obesity. "With obesity, PEDF release is
increased from fat, leading to higher levels of PEDF in the bloodstream," said
Matthew Watt of Monash University in Australia. "PEDF sends a signal to other body
tissues, causing insulin resistance in muscle and liver, a major defect that leads to the
development of type 2 diabetes." Elevated PEDF is also associated with increased
release of fatty acids from fat stores, which causes blood lipid levels to rise. That
"dyslipidemia" may be associated with other complications including
cardiovascular disease. What's more, they found that treatments designed to block the
action of PEDF in obese mice lowered the animals' blood lipid levels and reversed some of
their insulin resistance, Watt said. In recent years, scientists have come to appreciate
fat cells as important regulators of metabolism, at least in part through the hormones and
other chemicals they secrete. Changes in fat-cell size are also accompanied by
reprogramming of the fat-cell secretory profile, a shift that is thought to play an
important role in the link between obesity and insulin resistance, the researchers said.
That has led scientists in search of all the chemicals issued by fat tissuethe
so-called adipocyte secretomein hopes of identifying regulatory players with
as-yet-unidentified roles in whole-body metabolism.

According to a research abstract that will be presented on Monday, June 8 at SLEEP 2009,
the 23rd Annual Meeting of the Associated Professional Sleep Societies, in the presence of
free access to food, sleep restricted subjects reported decrease in appetite, food
cravings and food consumption; however, they gained weight over the course of the study.
Thus, the finding suggests that energy intake exceeded energy expenditure during the sleep
restriction Results indicate that people whose sleep was restricted experienced an average
weight gain of 1.31 kilograms over the 11 days of the study. Of the subjects with
restricted sleep who reported a change in their appetite and food consumption, more than
70 percent said that it decreased by day 5 of the study. A group of well rested control
subjects did not experience the weight gain. According to lead investigator Siobhan Banks,
PhD, a research fellow at the University of South Australia and former assistant research
professor at the University of Pennsylvania School of Medicine, it was surprising that
participants did not crave foods rich in carbohydrates after sleep restriction, as
previous research suggested they might. Results indicate that even though physiologically
the desire to eat was not increased by sleep loss in participants, other factors such as
the sedentary environment of the laboratory and the ability to snack for longer due to
reduction in time spent asleep might have influenced the weight gain.

Individuals who are overweight or
obese in mid-life have a greater risk of reduced memory and thinking skills in late life

Individuals with higher mid-life Body Mass Index (BMI) in the 1960s have been found to
have lower memory and thinking skills and a sharper decline in these abilities in old age,
compared to those with lower BMI in mid-life. The adverse effects of being
overweight and obese are not limited to cardiac function, but also extend to brain
function, says Anna Dahl doctoral student at the School of Health Sciences,
JŲnkŲping. Several studies, including studies from the Swedish Twin Registry, have shown
that individuals who are overweight or obese in mid-life are at an increased risk of
suffering from dementia. We have extended this knowledge and shown that being
overweight or obese in mid-life also negatively affects memory and thinking skills
independent of dementia. Moreover, these skills decline more rapidly in old age among
those who were overweight or obese in mid-life, writes Anna Dahl in an article
published in the Journal of Gerontology. The steeper decline in memory and thinking
skills observed among individuals who were overweight or obese in mid-life, cannot be
explained in our study by an increased prevalence of cardiovascular diseases, says
Anna Dahl. There are probably other mechanisms that explain this link.

Many conventional media sources, known collectively as Mainstream Media, or
MSM, repeat the conventional wisdom of obesitys causes: sedentary lifestyle and poor
nutrition. These factors are irrefutable contributors to the worldwide, growing obesity
epidemic. Yet lifestyle and nutrition factors do not tell the whole story. There are much
more nuanced and insidiously dangerous implications in the massive increase in obesity:
connections to rising cancer rates, and correlations to stored body toxicity. This article
illustrates the growing evidence linking this unholy triad of obesity, cancer,
and toxicity.

The Nordic diet is one of the latest diets to come along that involves foods from a
certain region and their health benefits. The Nordic diet is a diet that is rich in
rapeseed oil, elk and cowberries. It is considered to be more suitable for those who live
in Northern climates than the traditional Mediterranean diet.

Many animals live longer when raised on low calorie diets. But now researchers at
Washington University School of Medicine in St. Louis have shown that they can extend the
life spans of roundworms even when the worms are well fed  it just takes a chemical
that blocks their sense of smell. Three years ago, the researchers, led by Kerry Kornfeld,
M.D., Ph.D., reported they found that a class of anticonvulsant medications made the
roundworm Caenorhabditis elegans live longer. But until now, they didn't quite know what
the drugs did to give the worms their longevity. They report their latest findings in the
Oct. 24 issue of the Public Library of Science Genetics. "We've learned that the
drugs inhibit neurons in the worm's head that sense chemicals in their surroundings 
the neurons are like the worm's nose," says Kornfeld, professor of developmental
biology. "Like roundworms that are grown in a food-scarce environment, the worms
exposed to the anticonvulsant ethosuximide lived longer. But these worms ate plenty of
food. That suggests that the worms' sensation of food is critical to controlling their
metabolism and life span." If roundworms sense that food is abundant, their
metabolism adjusts accordingly. Their bodies respond to promote rapid ingestion, rapid
growth and rapid aging, Kornfeld explains. In contrast, when the worms sense a shortage of
food, they make "metabolic decisions" to delay growth, delay energy use and
extend lifespan.In the long term, Kornfeld's goal is to identify compounds that could
potentially delay human aging. The research group for this project also included James
Collins, Ph.D., Kim Evason, M.D., Ph.D., Chris Pickett, Ph.D., and Daniel Schneider.
Kornfeld's lab studies C. elegans because they live only about two to three weeks, so
experimental results can be obtained quickly. In addition, the worms' genome has been
sequenced and extensively studied.

Don't feel like you are getting full when eating a large meal? New research from The
Miriam Hospital suggests that a physiological response may partially explain why severely
obese individuals may not feel satisfied after eating and often have difficulty
controlling the amount of food they consume during a meal. Researchers led by Dale Bond,
PhD, of The Miriam Hospital's Weight Control and Diabetes Research Center focused on
habituation, or the idea that continual exposure to a specific food decreases one's
physical response to that food. Habituation theory suggests that if one habituates, or
adjusts, slowly to food cues, they are less likely to feel satisfied with that particular
food and can consume more of it. In the study, published online in Obesity Surgery, the
research team looked at saliva production following repeated exposure to lemon juice. They
compared the responses of two groups  severely obese patients preparing for
bariatric surgery and normal weight individuals  and found that the bariatric
surgery candidates continued to salivate at a consistent rate throughout the tastings,
indicating that very little habituation occurred. Meanwhile, the salivation rate of the
normal weight controls decreased with successive exposures to the lemon juice. "The
failure of bariatric surgery candidates to habituate suggests that satiation, or the
feeling of fullness while eating, is impaired in this population. This could play a role
in the inability of some severely obese individuals to regulate or control the amount of
food that they eat during a meal," says Bond. He adds that the findings make a case
for the use of habituation as a model to study why some patients who have undergone
bariatric surgery continue to engage in problematic behaviors, such as binge eating, which
contributes to poorer weight loss outcomes. The study included 34 severely obese bariatric
surgery candidates and 18 individuals of normal weight. Saliva was collected from cotton
balls positioned in each participant's mouth during two baseline water trials and ten
lemon juice trials. Participants also completed questionnaires to assess the level of
conscious control over eating as well as the frequency of binge eating episodes during the
previous 28 days.

According to trials, a new obesity drug, Tesofensine, which may be launched on the world
market in a few years, can produce weight loss twice that of currently approved obesity
drugs. The Danish company Neurosearch and a number of researchers at the Faculty of Life
Sciences at University of Copenhagen are behind the promising findings. Tesofensine can
produce weight loss twice that of currently approved obesity drugs, and should be studied
in phase III trials. These are the conclusions of an Article published early Online and in
an upcoming edition of The Lancet, written by Professor Arne Astrup, Department of Human
Nutrition, Faculty of Life Sciences, University of Copenhagen, Denmark, and colleagues.
Increased obesity prevalence worldwide, in both developed and developing countries,
results in more people with cardiovascular disease, diabetes, musculoskeletal disorders,
and cancer. Whilst gastric bypass surgery substantially reduces bodyweight and
obesity-related disease, the researchers believe a treatment gap exists between the
effectiveness of currently marketed obesity drugs and gastric-bypass surgery. Tesofensine
 which inhibits the presynaptic uptake of the neurotransmitters noradrenaline,
dopamine and serotonin in the brain  has been shown to be safe and effective in
animal models. It also caused unintended weight loss when it was given obese patients with
Parkinson's or Alzheimer's disease when it was researched for those conditions. The drug
works by suppressing hunger, leading to an energy deficit which burns off excess body fat.
This randomised, placebo-controlled phase II study was done in five Danish obesity
management centres, and involved 203 obese patients (body mass index 30-40 kg/m2),
weighing a mean of just over 100kg. They were prescribed a limited-energy diet and
assigned to tesofensine 0.25mg (52 patients), 0.5 mg (50), 1.0 mg (49), or placebo (52),
all once daily for 24 weeks. The primary outcome was percentage change in bodyweight. A
total of 161 patients completed the study, and an analysis showed that the mean weight
loss recorded for placebo and diet was 2.2kg and for tesofensine 0.25mg, 0.5mg and 1.0mg
it was 6.7kg, 11.3kg, and 12.8kg respectively. For the 0.5mg and 1.0mg doses, this
represented a weight loss around twice that attained using sibutramine or rimonabant*, the
currently-approved therapies in Europe. Blood pressure was increased in the 1.0mg
group.The most common side-effects caused by tesofensine were dry mouth, nausea,
constipation, hard stools, diarrhoea, and insomnia. The authors conclude that the 0.5mg
dose of tesofensine is more promising than the 1.0mg dose because it produces a similar
weight loss with less side-effects. They say: "We conclude that tesofensine 0.5 mg,
once daily for 6 months, has the potential to produce twice the weight loss as currently
approved drugs; however, larger phase III studies are needed to substantiate our
findings."

Possible anti-obesity effects of white tea have been demonstrated in a series of
experiments on human fat cells (adipocytes). Researchers writing in BioMed Central's open
access journal Nutrition and Metabolism have shown that an extract of the herbal brew
effectively inhibits the generation of new adipocytes and stimulates fat mobilization from
mature fat cells. Marc Winnefeld led a team of researchers from Beiersdorf AG, Germany,
who studied the biological effects of an extract of white tea  the least processed
version of the tea plant Camellia sinensis. He said, "In the industrialized
countries, the rising incidence of obesity-associated disorders including cardiovascular
diseases and diabetes constitutes a growing problem. We've shown that white tea may be an
ideal natural source of slimming substances". After treating lab-cultured human
pre-adipocytes with the tea extract, the authors found that fat incorporation during the
genesis of new adipocytes was reduced. According to Winnefeld, "The extract solution
induced a decrease in the expression of genes associated with the growth of new fat cells,
while also prompting existing adipocytes to break down the fat they contain". White
tea is made from the buds and first leaves of the plant used to make green tea and the
black tea most commonly drunk in Western countries. It is less processed than the other
teas and contains more of the ingredients thought to be active on human cells, such as
methylxanthines (like caffeine) and epigallocatechin-3-gallate (EGCG)  which the
authors believe to be responsible for many of the anti-adipogenic effects demonstrated in
their study.

The world-wide explosion of overweight people has been called an epidemic. The
inflammatory nature of obesity is widely recognized. Could it really be an epidemic
involving an infectious agent? In this climate of concern over the increasing prevalence
of overweight conditions in our society, investigators have focused on the possible role
of oral bacteria as a potential direct contributor to obesity. To investigate this
possibility, the study's researchers J.M. Goodson, D. Groppo, S. Halem and E. Carpino
measured salivary bacterial populations of overweight women. Saliva was collected from 313
women with a body mass index between 27 and 32, and bacterial populations were measured by
DNA probe analysis. Levels in this group were compared with data from a population of 232
healthy individuals from periodontal disease studies. The median percentage difference of
seven of the 40 bacterial species measured was greater than 2 percent in the saliva of
overweight women. Classification tree analysis of salivary microbiological composition
revealed that 98.4 percent of the overweight women could be identified by the presence of
a single bacterial species (Selenomonas noxia) at levels greater than 1.05 percent of the
total salivary bacteria. Analysis of these data suggests that the composition of salivary
bacteria changes in overweight women. It seems likely that these bacterial species could
serve as biological indicators of a developing overweight condition. Of even greater
interest, and the subject of future research, is the possibility that oral bacteria may
participate in the pathology that leads to obesity.

Why the average physically inactive
person should eat a Mediterranean diet

If you are a health conscious person physical activity is part of daily life. Unless you
get injured, most people who regularly perform some physical activity enjoy it because it
helps them keep fit and feel great. Conversely, health conscious people like their fruits
and veggies and eat a healthy diet. But what if you get injured? Or are starting out a
workout routine, having been physically inactive for some time? According to a recent
study published by the Public Library of Science, the first step would be to eat a
Mediterranean diet.

The machinery responsible for energy production in fat cells is working poorly as a result
of obesity. This may aggravate and work to maintain the obese state in humans, suggests
the recent Finnish study. Studying rare cases of young identical twins with large
differences in bodyweight a Finnish research group has shown that already in the very
early stages of obesity, clear changes in the function of the cellular mitochondria can be
observed.

Protein intake is key to weight
management after weight loss concludes the DIOGENES 8 European country dietary
intervention study

"Protein intake holds the key to effective weight maintenance after weight
loss," stated Professor Arne Astrup of the University of Copenhagen and Co-ordinator
of the EC-funded Diogenes diet and weight regain prevention study, today at the Diogenes
Symposium (Tuesday 5th May 2009, The Netherlands). Professor Astrup continued "Taking
all 8 centres together and the results from 548 adults, we are able to see that those
subjects randomised to the higher protein diet after weight loss were able to maintain
that weight loss most successfully. Some subjects randomised to the lower glycemic index
(GI) diet also had some success with weight maintenance but it was less marked than those
on the higher protein diet. 548 adult subjects completed the study with clinical
measurements taken on three different occasions (i) before the weight loss period (when at
least 8% of initial bodyweight had to be lost); (ii) end of weight loss and prior to
dietary intervention period and (iii) end of 6 month intervention period. The aim for the
diets was a difference in protein intake of > 10 energy% and in GI of > 10 units.
Two centres provided subjects with all foods for free using a shop system and 6 centres
provided dietary instruction only to subjects. Subjects also undertook tests that have fed
into other aspects of the Diogenes study. Professor Astrup continued "This study
confirms the view that the diet chosen after weight loss does help with weight
maintenance, contrary to other recently released studies which concluded that the diet
makes no difference. We can have confidence in our findings and conclusions as each
subject was closely monitored during the study and there was a much lower drop-out rate in
the high protein group - possibly due to successful weight management during the study
period."

Genetically engineered mice don't
get obese, but do develop gallstones

Obesity and gallstones often go hand in hand. But not in mice developed at Washington
University School of Medicine in St. Louis. Even when these mice eat high-fat diets, they
don't get fat, but they do develop gallstones. Researchers say the findings offer clues
about genetic factors related to gallstones, and they believe better understanding of
those factors may one day allow physicians to monitor people at risk and even, perhaps, to
intervene before gallstones become a serious problem. Learning more about susceptibility
to gallstones is an important public health issue, particularly in the United States.
Between 16 million and 22 million Americans have gallstones, which are deposits of
cholesterol or calcium salts that form in the gallbladder or in the bile ducts. In many
cases, people require surgery, and more than half a million undergo operations to treat
gallstones and remove the gallbladder each year.

Angiotensin 1-7, a hormone in the body that has cardiovascular benefits, improves the
metabolic syndrome in rats, according to a new study. The results will be presented
Wednesday at The Endocrine Society's 91st Annual Meeting in Washington, D.C. "No
specific form of medical therapy for the metabolic syndrome presently exists," said
the study's lead author, Yonit Marcus, MD, a PhD student at the Weizmann Institute of
Science in Rehovot, Israel. "But an estimated 20 to 25 percent of the world's adult
population has the metabolic syndrome." The metabolic syndrome is a cluster of risk
factors that raise the risk of developing heart disease, stroke and diabetes. A diagnosis
of the metabolic syndrome comes from having at least three of the following: increased
waist circumference (abdominal obesity), low HDL ("good") cholesterol, high
triglycerides (fats in the blood), high blood pressure and high blood glucose (blood
sugar). The renin-angiotensin system and its key player, the hormone angiotensin II,
normally help control blood pressure, but when overactive, this hormone likely contributes
to the development of obesity and the metabolic syndrome. A product of angiotensin II
metabolism, a hormone called angiotensin 1-7, counteracts many of the negative effects of
excess angiotensin II, including high blood pressure, kidney disease, heart failure and
cardiac arrhythmia (abnormal heart rhythms), according to Marcus. With the other
researcheres, Marcus examined whether angiotensin 1-7 has a beneficial effect on the
metabolic syndrome, using an established model of the syndrome, "the fructose-fed
rat." In this model, rats are fed a diet heavy in fructose sweetener, and over time
they develop similar characteristics to the human metabolic syndrome.

Older women who take hormone therapy to relieve menopausal symptoms may get the added
benefit of reduced body fat if they are physically active, according to a new study. The
results were presented at The Endocrine Society's 91st Annual Meeting in Washington, D.C.
The study provides new information on the health benefits of any type of physical
activity, not just exercise, said the presenting author Poli Mara Spritzer, MD, PhD, a
professor at the Federal University of Rio Grande do Sul in Porto Alegre, Brazil, and
chief of the Gynecological Endocrinology Unit at the university's Hospital de Clinicas de
Porto Alegre. After menopause, a woman's percentage of body fat tends to increase and
redistribute to the abdomen, Spritzer said. Excess belly fat is a risk factor for diabetes
and heart disease. Postmenopausal women who exercise have a lower percentage of body fat
than sedentary women, past research shows. However, Spritzer said less is known about the
influence on body fat composition of physical activity in women receiving hormone
replacement therapy, or HRT. Some data suggest that estrogen treatment may add to the
effect of exercise in reducing fat. Spritzer and her colleagues studied 34 healthy women
who had an average age of 51 years, had experienced menopause for less than 3 years and
sought HRT to relieve hot flashes, night sweats and vaginal dryness. They evaluated the
women's cholesterol levels, body mass index (BMI), waist circumference (a measure of
abdominal fat) and percentage of body fat before and after 4 months of HRT. The women
received estrogen plus progesterone therapy in either non-oral (nasal and vaginal) or
low-dose oral preparations. For 6 consecutive days before starting HRT and 6 days at the
end of HRT, women wore a pedometer to estimate their level of physical activity. The
device measured the steps they took, including walking, working, and doing house chores
and leisure activities. They were instructed to not change their usual activities. Most of
the women did not play sports or do any structured physical exercise, according to
Spritzer. Results showed that 24 of the women were physically activedefined as
taking 6,000 steps or more per dayand 10 were inactive (less than 6,000 steps a
day). For a woman who has a step, or stride, length of 2 feet (60 cm), 6,000 steps would
be around 2.25 miles (3.6 km), Spritzer estimated. For active women, the higher the number
of steps they took, the lower was their waist measurement and the better their level of
"good" (high-density-lipoprotein, or HDL) cholesterol, the authors reported. The
inactive women did not have any changes in body fat or cholesterol. However, when all 34
women were considered in the analysis, body fat still declined significantly after HRT.

New research suggests that, if used properly, vibration plate exercise machines may help
you lose weight and trim the particularly harmful belly fat between the organs. In a study
presented on Friday at the European Congress on Obesity, scientists found that overweight
or obese people who regularly used the equipment in combination with a calorie restricted
diet were more successful at long-term weight loss and shedding the fat around their
abdominal organs than those who combined dieting with a more conventional fitness routine.
"These machines are increasingly found in gyms across the industrialized world and
have gathered a devoted following in some places, but there has not been any evidence that
they help people lose weight. Our study, the first to investigate the effects of vibration
in obese people, indicates it's a promising approach. It looks like these machines could
be a useful addition to a weight control package," said the study's leader, Dirk
Vissers, a physiotherapist at the Artesis University College and the University of Antwerp
in Belgium. Vissers and his colleagues studied the effects of the Power Plate in 61
overweight or obese people - mostly women - for a year. The intervention lasted six
months, after which the scientists advised all the volunteers to do the best they could
with a healthy diet and exercise regime on their own for another six months. Body
measurements, including CT scans of abdominal fat, were taken at the beginning of the
study and after three, six and 12 months. The researchers divided the volunteers into four
groups. One group was prescribed an individually calculated calorie restricted diet.
Dietician visits were scheduled every fortnight for the first three months and every month
for the second three months. The dieters were asked not to engage in any exercise for the
duration of the six-month intervention. A second group received the same diet
intervention, with the addition of a conventional fitness regime. They attended supervised
exercise classes twice a week for an hour and were urged to exercise on their own a third
time each week. The sessions included group cycling, swimming, running, step aerobics and
some general muscle strengthening exercises. A third group got the diet intervention plus
supervised vibration plate training instead of conventional exercise. They were asked not
to do any aerobic exercise during the six-month intervention phase. The physiotherapists
gradually increased the speed and intensity of the machine each week, as well as the
variety and duration of the exercises from 30 seconds for each of 10 exercises to 60
seconds for each of 22 exercises, such as squats, lunges, calf raises, push-ups and
abdominal crunches. The average time spent on the machine was 11.9 minutes per session in
the first three months and 14.2 minutes in the second three months. A fourth group got no
intervention. There were no significant differences between the groups in obesity and
abdominal, or visceral, fat at the start of the study. "Over the year, only the
conventional fitness and vibration groups managed to maintain a 5% weight loss, which is
what is considered enough to improve health," Vissers said.

One year after giving birth, women were less likely to have the most dangerous kind of
obesity if they had been given probiotics from the first trimester of pregnancy, found new
research that suggests manipulating the balance of bacteria in the gut may help fight
obesity. Probiotics are bacteria that help maintain a healthy bacterial balance in the
digestive tract by reducing the growth of harmful bacteria. They are part of the normal
digestive system and play a role in controlling inflammation. Researchers have for many
years been studying the potential of using probiotic supplementation to address a number
of intestinal diseases. More recently, obesity researchers have started to investigate
whether the balance of bacteria in the gut might play a role in making people fat and
whether adjusting that balance could help. "The results of our study, the first to
demonstrate the impact of probiotics-supplemented dietary counselling on adiposity, were
encouraging," said Kirsi Laitinen, a nutritionist and senior lecturer at the
University of Turku in Finland who presented her findings on Thursday at the European
Congress on Obesity. "The women who got the probiotics fared best. One year after
childbirth, they had the lowest levels of central obesity as well as the lowest body fat
percentage." "Central obesity, where overall obesity is combined with a
particularly fat belly, is considered especially unhealthy," Laitinen said. "We
found it in 25% of the women who had received the probiotics along with dietary
counselling, compared with 43% in the women who received diet advice alone." In the
study, 256 women were randomly divided into three groups during the first trimester of
pregnancy. Two of the groups received dietary counselling consistent with what's
recommended during pregnancy for healthy weight gain and optimal foetal development. They
were also given food such as spreads and salad dressings with monounsaturated and
polyunsaturated fatty acids, as well as fibre-enriched pasta and breakfast cereal to take
home. One of those groups also received daily capsules of probiotics containing
Lactobacillus and Bifidobacterium, which are the most commonly used probiotics. The other
group received dummy capsules. A third group received dummy capsules and no dietary
counselling. The capsules were continued until the women stopped exclusive breastfeeding,
up to 6 months. The researchers weighed the women at the start of the study. At the end of
the study they weighed them again and measured their waist circumference and skin fold
thickness. The results were adjusted for weight at the start of the study. Central obesity
- defined as a body mass index (BMI) of 30 or more or a waist circumference over 80
centimetres - was found in 25% of the women who had been given the probiotics as well as
diet advice. That compared with 43% of the women who got dietary counselling alone and 40%
of the women who got neither diet advice nor probiotics. The average body fat percentage
in the probiotics group was 28%, compared with 29% in the diet advice only group and 30%
in the third group.

Increased food intake alone
explains the increase in body weight in the United States

New research that uses an innovative approach to study, for the first time, the relative
contributions of food and exercise habits to the development of the obesity epidemic has
concluded that the rise in obesity in the United States since the 1970s was virtually all
due to increased energy intake. How much of the obesity epidemic has been caused by excess
calorie intake and how much by reductions in physical activity has been long debated and
while experts agree that making it easier for people to eat less and exercise more are
both important for combating it, they debate where the public health focus should be. A
study presented on Friday at the European Congress on Obesity is the first to examine the
question of the proportional contributions to the obesity epidemic by combining metabolic
relationships, the laws of thermodynamics, epidemiological data and agricultural data.
"There have been a lot of assumptions that both reduced physical activity and
increased energy intake have been major drivers of the obesity epidemic. Until now, nobody
has proposed how to quantify their relative contributions to the rise in obesity since the
1970s. This study demonstrates that the weight gain in the American population seems to be
virtually all explained by eating more calories. It appears that changes in physical
activity played a minimal role," said the study's leader, Professor Boyd Swinburn,
chair of population health and director of the World Health Organization Collaborating
Centre for Obesity Prevention at Deakin University in Australia. The scientists started by
testing 1,399 adults and 963 children to determine how many calories their bodies burn in
total under free-living conditions. The test is the most accurate measure of total calorie
burning in real-life situations. Once they had determined each person's calorie burning
rate, Swinburn and his colleagues were able to calculate how much adults needed to eat in
order to maintain a stable weight and how much children needed to eat in order to maintain
a normal growth curve. They then worked out how much Americans were actually eating, using
national food supply data (the amount of food produced and imported, minus the amount
exported, thrown away and used for animals or other non-human uses) from the 1970s and the
early 2000s. The researchers used their findings to predict how much weight they would
expect Americans to have gained over the 30-year period studied if food intake were the
only influence. They used data from a nationally representative survey (NHANES) that
recorded the weight of Americans in the 1970s and early 2000s to determine the actual
weight gain over that period.

The antibody works against the gastric hormone ghrelin (pronounced "grell-in"),
which has been linked to weight gain and fat storage through its metabolic actions. These
findings point towards a potentially novel treatment for obesity that would interfere
directly with the some of the biological mechanisms determining weight. The study is being
published the week of October 27, 2008, in an advance, online Early Edition of the journal
Proceedings of the National Academy of Sciences (PNAS). In the study, which was led by
investigators Kim Janda and Eric P. Zorrilla of The Scripps Research, the antibody
catalyst GHR-11E11 led to a higher metabolic rate in fasting mice and suppressed feeding
following 24-hour food deprivation. "Our study showed that this novel catalytic
ghrelin antibody could specifically seek out and degrade ghrelin," said Janda, who is
Ely R. Callaway, Jr. Professor of Chemistry, member of The Skaggs Institute for Chemical
Biology, and director, Worm Institute of Research and Medicine (WIRM), at Scripps
Research. "While this antibody lacks a high level of catalytic efficiency, our study
clearly demonstrates that even a basal level of catalysis can effectively modulate feeding
behavior. These findings not only validate antibody-based therapeutics, but strongly
suggest that catalytic anti-ghrelin antibodies might help patients reach and maintain
their weight loss goals." According to recent reports from the World Health
Organization, about 1 billion people worldwide are overweight or obese, with most of these
in the developed world. In the United States, for example, the National Health and
Nutrition Examination Survey found that, in 2003-2004, approximately 66 percent of all
adults 20 years of age or older were overweight or obese. Almost four out of every five
American men aged 40 to 59 were classified as overweight, according to a 2006 study
published by the Journal of the American Medical Association. While non-surgical
treatments can be modestly effective against obesity, weight loss or gain can be affected
by ghrelin, which is released by the body to encourage eating during periods of calorie
restriction. A gastric endocrine hormone produced primarily in the stomach, ghrelin
promotes weight gain and fat storage through its metabolic actions, decreasing the break
down of stored fat for energy as well as energy expenditure itself.

Body mass index (BMI) varies as a function of habitual sleep duration, according to a
research abstract that will be presented on Thursday, June 11, at SLEEP 2009, the 23rd
Annual Meeting of the Associated Professional Sleep Societies. Results indicate that twins
who slept between 7 and 8.9 hours each night had a lower mean BMI (25.0 kg/m2) compared to
those who regularly slept either more (25.2 kg/m2) or less (26.4 kg/m2) per night. The
relationship between sleep duration and BMI remained significant after controlling for
genetics and shared environment. According to lead author Nathaniel Watson, MD,
co-director at the University of Washington Sleep Institute in Seattle, sleep habits have
a significant impact on weight and BMI. Findings of the study point towards an
environmental cause of the relationship between sleep duration and BMI, said Watson.
Results were robust enough to be present when the sample was limited to identical
twins. The study involved data from 1,797 twins, including 634 twin pairs (437
monozygotic, 150 dizygotic and 47 indeterminate pairs) and 529 individual twins with a
mean age of 36.8 years. Habitual sleep duration was obtained by self-reported length of
sleep per night, and BMI was calculated by self-reported height and weight. Of the sample,
68.3 percent was female, and 88.2 percent was Caucasian. Results persisted in a co-twin
control analysis of within twin pair differences in sleep duration and BMI.

Everyone seems to feel that lack of physical activity and improper nutrition are the
reason why children and adults are so obese. However, some feel that while lifestyle
choices such as eating unhealthy foods and not exercising may contribute to obesity,
chemical exposure can be a huge factor when it comes to increasing weight in both children
and adults.

Scientists have determined that a specific gene plays a role in the weight-gain response
to a high-fat diet. The finding in an animal study suggests that blocking this gene could
one day be a therapeutic strategy to reduce diet-related obesity and associated disorders,
such as diabetes and liver damage, in humans.The researchers found that a diet rich in fat
induced production of this gene, called protein kinase C beta (PKC beta), in the fat cells
of mice. These mice rapidly gained weight while eating a high-fat diet for 12 weeks.

There is no "one size fits all" when it comes to weight loss through exercise,
says Queensland University of Technology behavioral scientist Neil King. Dr. Neil King,
from QUT's Institute of Health and Biomedical Innovation, is the lead author of a study
conducted in collaboration with the University of Leeds in the UK, which has been
published in the latest edition of the International Journal of Obesity.

As millions of Americans gear up for the Thanksgiving holiday, a new report published
online in the FASEB Journal, may provide some relief for those leery second helpings.
Researchers describe a discovery that may allow some obese people avoid common
obesity-related metabolic problems without losing weight: they make a common antioxidant,
melanin, in excess. Even more promising is that some of the antioxidant drugs that can
mimic the melanin effect are FDA-approved and available.

It's called the obesity paradox. Although obese people are more apt to suffer from
inflammatory diseases, such as diabetes, heart disease, and stroke, they are also more
likely to survive a major attack caused by one of those conditions. University of Illinois
scientists Gregory Freund and Christina Sherry shed light on the reasons for this
phenomenon in a study in this month's issue of Endocrinology. "Fat is a very complex
and active tissueit has important functions beyond providing energy and insulating
us from the cold," said Freund, a professor in the U of I College of Medicine's
Department of Pathology and a faculty member in the U of I Division of Nutritional
Sciences. "We now know that leptin, a hormone secreted by fat tissue, plays a key
role in regulating the immune system. When we exposed mice to hypoxia (simulating an
event, such as a heart attack, in which a part of the body is deprived of oxygen), leptin
triggered the immune system to increase production of an anti-inflammatory molecule,
interleukin-1 receptor antagonist (IL-1RA)," he said. "And, when we gave
non-obese mice leptin injections, they recovered three times faster. Leptin did not hasten
recovery though in IL-1RA knockout mice," Sherry said. That earlier work was
published in a recent issue of Brain, Behavior, and Immunity.

A flavonoid derived from citrus fruit has shown tremendous promise for preventing weight
gain and other signs of metabolic syndrome which can lead to Type 2 Diabetes and increased
risk of cardiovascular disease. The study, led by Murray Huff of the Robarts Research
Institute at The University of Western Ontario looked at a flavonoid (plant-based
bioactive molecule) called naringenin. The findings are published online in the journal
Diabetes. In the study one group of mice was fed a high-fat (western) diet to induce the
symptoms of metabolic syndrome. A second group was fed the exact same diet and treated
with naringenin. Naringenin corrected the elevations in triglyceride and cholesterol,
prevented the development of insulin resistance and completely normalized glucose
metabolism. The researchers found it worked by genetically reprogramming the liver to burn
up excess fat, rather than store it. "Furthermore, the marked obesity that develops
in these mice was completely prevented by naringenin," says Huff, Director of the
Vascular Biology Research Group at Robarts and Professor of Medicine and Biochemistry at
the Schulich School of Medicine & Dentistry. "What was unique about the study was
that the effects were independent of caloric intake, meaning the mice ate exactly the same
amount of food and the same amount of fat. There was no suppression of appetite or
decreased food intake, which are often the basis of strategies to reduce weight gain and
its metabolic consequences." While grapefruit has long been linked to weight loss
diets, the concentrations of the citrus-derived flavonoid being studied are at higher
levels than you could get from dietary components. "We are examining the
pharmacological properties of naringenin," explains Huff. "The next step is to
find out if naringenin prevents heart disease in animal models and to explore the
feasibility of clinical trials to determine its safety and efficacy in humans." This
study investigated naringenin's preventative properties, but Huff is also investigating
whether it can treat obesity and other existing metabolic problems. "These studies
show naringenin, through its insulin-like properties, corrects many of the metabolic
disturbances linked to insulin resistance and represents a promising therapeutic approach
for metabolic syndrome."

Like father, like son -- new research points to gender relationships between parents and
their children as vital factor in childhood obesity. The relationships between children
and their parent of the same gender in the earliest years of life could be the key to
understanding why some young people become obese and others do not, new research conducted
by the EarlyBird Diabetes Study has shown. A study published today in the International
Journal of Obesity indicates that girls whose mothers are classified as clinically obese
are significantly more likely to struggle with weight problems in childhood, with a
similar relationship existing between obese fathers and their sons. The findings showed
that the same trend does not exist between mothers and their sons and fathers and their
daughters  meaning that behavioural, rather than genetic, factors could be the key
to unravelling the causes of the current obesity epidemic affecting children in the UK.

New research from the University of Illinois suggests that weight-loss campaigns that
promote exercise may actually cause people to eat more. People who viewed posters
suggesting that they "join a gym" or "take a walk" ate more food after
looking at the posters than people who saw similarly designed posters prompting them to
"make friends" or "be in a group," the researchers found. Subliminal
words about being active had a similar effect on study participants, said psychology
professor Dolores AlbarracŪn, who led the research. "Viewers of the exercise
messages ate significantly more (than their peers, who viewed other types of
messages)," she said. "They ate one-third more when exposed to the exercise
ads." Those exposed to subliminal words about activity during a computer task ate
about 20 percent more than those exposed to neutral words, she said. The study, which
appears in the journal Obesity, builds on previous research by AlbarracŪn that suggests
that general messages to be active can prompt people to behave in a variety of ways, some
of which may have negative consequences.

Obesity has become an epidemic in many parts of the western hemisphere; over 30 % of the
population of Germany are overweight. Scientists from the University of Cologne, in
cooperation with scientists from the University of DŁsseldorf, have been able to verify
the relevance of a certain gene with regard to obesity for the first time. The results of
this work have been published in the international journal of science, Nature. In 2006,
scientists discovered increased amounts of variations of the FTO genes were in overweight
people. However, the relevance of this gene and its regular function remained unclear for
a long time. The team working for Prof. Dr. Jens BrŁning, coordinator of the Cluster of
Excellence "Cellular Stress Responses in Aging-Associated Diseases", CECAD
Cologne, and Prof. Dr. Ulrich RŁther, University of DŁsseldorf, have now been able to
show that mice which do not have FTO gene, do not become overweight and burn more energy.
These findings verify the importance of the FTO gene for the regulation of body weight.
The results of this research will become very important for the development of new ways of
treating obesity

Keeping your baby fat turns out to be a good thing, as long as it is "brown
fat"the kind that burns calories, according to a study that found adults have
much more of this type of fat than previously thought. The results, which suggest a new
way to treat obesity, were presented at The Endocrine Society's 91st Annual Meeting in
Washington, D.C. Brown fat burns off calories and generates heat in babies and small
mammals. Most of our body fat is white fat, which also provides insulation but stores
calories. It becomes "bad" fat when you have too much. The "good"
fatbrown fatwas considered essentially nonexistent in human adults. "We
now know that it is present and functional in adults," said the study's lead author,
Aaron Cypess, MD, PhD, MMSc, of the Joslin Diabetes Center in Boston. "Three ounces
of brown fat can burn several hundred calories a day." For the first time, the
researchers were able to measure patches of brown adipose tissuebrown fatin
people, thanks to a high-tech imaging method that combines positron emission tomography
and computed tomography, called PET/CT. By evaluating biopsy tissue of what appeared to be
brown fat on PET/CT scans in some patients who had neck surgery, the authors confirmed
that they were, indeed, looking at stores of brown fat. More than 1,970 study participants
had PET/CT scans, from mid-skull to mid-thigh.

Vitamin D levels in the body at the start of a low-calorie diet predict weight loss
success, a new study found. The results, which suggest a possible role for vitamin D in
weight loss, were presented at The Endocrine Society's 91st Annual Meeting in Washington,
D.C. "Vitamin D deficiency is associated with obesity, but it is not clear if
inadequate vitamin D causes obesity or the other way around," said the study's lead
author, Shalamar Sibley, MD, MPH, an assistant professor of medicine at the University of
Minnesota. In this study, the authors attempted to determine whether baseline vitamin D
levels before calorie restriction affect subsequent weight loss. They measured circulating
blood levels of vitamin D in 38 overweight men and women before and after the subjects
followed a diet plan for 11 weeks consisting of 750 calories a day fewer than their
estimated total needs. Subjects also had their fat distribution measured with DXA (bone
densitometry) scans. On average, subjects had vitamin D levels that many experts would
consider to be in the insufficient range, according to Sibley. However, the authors found
that baseline, or pre-diet, vitamin D levels predicted weight loss in a linear
relationship. For every increase of 1 ng/mL in level of 25-hydroxycholecalciferolthe
precursor form of vitamin D and a commonly used indicator of vitamin D
statussubjects ended up losing almost a half pound (0.196 kg) more on their
calorie-restricted diet. For each 1-ng/mL increase in the active or "hormonal"
form of vitamin D (1,25-dihydroxycholecalciferol), subjects lost nearly one-quarter pound
(0.107 kg) more. Additionally, higher baseline vitamin D levels (both the precursor and
active forms) predicted greater loss of abdominal fat. "Our results suggest the
possibility that the addition of vitamin D to a reduced-calorie diet will lead to better
weight loss," Sibley said.

A team of Australian researchers have developed a novel way to control the extreme weight
loss, common in late-stage cancer, which often speeds death. The findings published today
in Nature Medicine suggest it may soon be possible to prevent this condition, giving
people the strength to survive treatment and improve their chances of recovery.

A modest reduction in the amount of carbohydrates eaten, without calorie restriction and
weight loss, appears to increase a sense of fullness, which may help people eat less, a
preliminary study found. The results were presented at The Endocrine Society's 91st Annual
Meeting in Washington, D.C. "There has been great public interest in low-carbohydrate
diets for weight loss, but they are difficult to maintain, in part because of the drastic
reduction in carbohydrates," said coauthor Barbara Gower, PhD, a professor in the
Department of Nutrition Sciences, University of Alabama at Birmingham. In this study
funded by the National Institutes of Health, Gower and her co-workers investigated whether
a modest reduction in dietary carbohydrates, or "carbs," would improve feelings
of fullness better than a carbohydrate level comparable to that of the typical U.S. diet.
In a standard American diet, according to Gower, 55 percent of daily calories consumed
come from carbohydrates: sugars, starches and fiber. The control diet used in their study
contained 55 percent of daily calories from carbohydrates, in contrast to their
"moderate-carb diet" which was 43 percent of calories from carbohydrates. The
moderate-carb diet had more fat than their control diet39 percent versus 27 percent
of caloriesso that protein intake could be the same percentage. The researchers
matched the protein intake of both diets studied (18 percent of calories) because protein
may influence both satiety ("fullness") and insulin secretion. The authors
assigned the moderate-carb diet to 16 adults and the standard diet to 14 adults for a
month. Subjects received enough calories to maintain their weight at what it was before
the study. During the study they were weighed each weekday, and if a participant gained or
lost weight, the amount of food was modified individually so weight could stay the same.
After the subjects adjusted to their diet for 4 weeks, they ate a test meal, a breakfast
that was specific to their diet.

Blocking a muscle growth-limiting
hormone protects against obesity and atherosclerosis

Knockout of myostatin, a growth factor that limits muscle growth, can decrease body fat
and promote resistance against developing atherosclerosis, or "hardening" of the
arteries, according to a new study conducted in mice. The results will be presented
Thursday at The Endocrine Society's 91st Annual Meeting in Washington, D.C. "Obesity
increases the risk of atherosclerosis, which accounts for 75% of all cardiovascular
events, such as heart attacks and strokes," said study co-author Shalender Bhasin,
MD, professor of medicine at Boston University School of Medicine and chief of the Section
of Endocrinology, Diabetes, and Nutrition at Boston Medical Center. "Current
strategies aimed at preventing heart disease consist primarily of lowering cholesterol
levels, but patients reaching the desired cholesterol levels are still at risk for
atherosclerosis if they have other risk factors, such as obesity." Humans and animals
with a mutation in the myostatin gene are extremely muscular and have little fat, past
research shows. Also, when the gene encoding myostatin is knocked out in mice, their
muscle mass increases. Bhasin and his co-workers wanted to find out if inhibiting
myostatin in mice could resist the development of diet-induced obesity and of
atherosclerosis, the buildup of lipid deposits called plaque that can narrow and clog
coronary arteries. The researchers took mice that were genetically altered to develop
atherosclerosis and then cross-bred them with myostatin knockout mice. Ten generations
later, they had mice who were genetically predisposed to both atherosclerosis and
inactivation of myostatin. For controls, they studied mice with a genetic predisposition
for atherosclerosis but with intact myostatin gene. All mice received a high-fat diet for
12 weeks, to spur the development of atherosclerosis.

Body Mass Index (BMI) varies as a function of habitual sleep duration, according to a
research abstract that will be presented on Thursday, June 11, at SLEEP 2009, the 23rd
Annual Meeting of the Associated Professional Sleep Societies. Results indicate that twins
who slept between 7 and 8.9 hours each night had a lower mean BMI (25.0 kg/m2) compared to
those who regularly slept either more (25.2 kg/m2) or less (26.4 kg/m2) per night. The
relationship between sleep duration and BMI remained after controlling for genetics and
shared environment. According to the lead author of the story, Nathaniel Watson, MD,
co-director at the University of Washington Sleep Institute, in Seattle, sleep habits have
a significant impact on weight and BMI. "Findings of the study point towards an
environmental cause of the relationship between sleep duration and BMI," said Watson.
"Results were robust enough to be present when the sample was limited to identical
twins." The study included data from 1,797 twins, including 634 twin pairs (437
monozygotic, 150 dizygotic and 47 indeterminate pairs) and 529 individual twins with a
mean age of 36.8. Habitual sleep duration was obtained by self-reported length of sleep
per night and BMI was calculated by self-reported height and weight. Of the sample, 68.3
percent female, 88.2 percent were Caucasian. Results persisted in a co-twin control
analysis of within twin pair differences in sleep duration and BMI.

When lean, healthy young adults gained about nine pounds, the functioning of their blood
vessel lining became impaired -- but shedding the weight restored proper functioning,
according to a Mayo Clinic research report.

Obese women have alterations in their ovaries which might be responsible for an egg's
inability to make an embryo, according to a new study accepted for publication in The
Endocrine Society's Journal of Clinical Endocrinology & Metabolism (JCEM). Obese women
trying to become pregnant experience longer times to conception, even if they are young
and have a regular menstrual cycle. This study sought to determine if there are
alterations in an egg's environment in obese women which contribute to poorer reproductive
outcomes. "Characteristics of eggs are influenced by the environment in which they
develop within the ovary," said Dr. Rebecca Robker, PhD, of Adelaide University in
Australia and lead author of the study. "Our study found that obese women have
abnormally high levels of fats and inflammation in the fluid surrounding their eggs which
can impact an egg's developmental potential." According to Dr. Robker, the fats might
alter the very sensitive metabolism of the egg and such changes are known to be harmful to
embryo formation. In addition, inflammation can damage cells and when this happens to eggs
it can affect embryo survival. For this study, researchers followed 96 women seeking
assisted reproduction at a private clinic in South Australia from February 2006 to April
2007. Dr. Robker and her colleagues measured hormone and metabolite levels in follicular
fluid obtained from the subjects' ovaries during their egg collection procedures. They
found that obese women exhibited an altered ovarian follicular environment, particularly
increased metabolite and androgen activity levels, which may be associated with poorer
reproductive outcomes. "Obesity is well known to cause changes in blood lipids and
heightened inflammation which detrimentally affects a person's general health," said
Dr. Robker. "Our research shows that obesity similarly changes the environment in the
ovary which bathes and nourishes a woman's developing eggs."

Obesity linked to hormone imbalance
that impacts sexual quality of life

Hormonal changes and diminished sexual quality of life among obese men are related to the
degree of obesity, and both are improved after gastric bypass surgery according to a new
study accepted for publication in The Endocrine Society's Journal of Clinical
Endocrinology & Metabolism (JCEM). "Previous studies have found that obesity is
correlated to lower sperm count and can be associated with infertility, but we wanted to
know if obesity was biologically associated with an unsatisfying sex life, and if so,
could it be reversible," said Dr. Ahmad Hammoud, MD, of the University of Utah and
lead author of the study. "Our results show that the answer to both questions may be
yes." For this study, researchers followed 64 men over two years who participated in
the Utah Obesity Study, which investigated the two-year morbidity of severely obese men
undergoing Roux-en-Y gastric bypass surgery compared to controls. Researchers measured
weight, BMI (body mass index) and reproductive hormone levels of participants at the
beginning of the study and once more two years later. Similarly subjects completed a
questionnaire designed to assess the impact of weight on quality of life in obese
individuals at the onset of the study and again two years later. "In our study
population, we found that lower testosterone levels and diminished ratings for sexual
quality of life were correlated with increased BMI," said Dr. Hammoud. "Subjects
who lost weight through bariatric surgery experienced a reduction in estradiol levels, an
increase in testosterone levels and an increase in ratings of sexual quality of
life."

It's a paradox that has flummoxed women for generations  their apparent ability to
store fat more efficiently than men, despite eating proportionally fewer calories. While
it has long been suspected that female sex hormones are responsible, a UNSW research
review has for the first time drawn a link between one hormone  oestrogen  and
its impact on fat storage for childbearing. On average, women have six to 11 percent more
body fat than men. Studies show oestrogen reduces a womans ability to burn energy
after eating, resulting in more fat being stored around the body. The likely reason is to
prime women for childbearing, the review suggests. "Female puberty and early
pregnancy  times of increased oestrogen  could be seen as states of efficient
fat storage in preparation for fertility, foetal development and lactation," the
studys author Associate Professor Anthony OSullivan, from UNSWs St
George Clinical School, said.

A research team led by Mitchell Lazar, MD, PhD, Director of the Institute for Diabetes,
Obesity, and Metabolism at the University of Pennsylvania School of Medicine, has used
state-of-the-art genetic technology to map thousands of positions where a molecular
master regulator of fat-cell biology is nestled in DNA to control genes in
these cells. The findings appear online this week in Genes & Development. The
international obesity epidemic is leading to major health risks, including increased rates
of diabetes, heart disease, and cancer. Obesity is caused by increased numbers of fat
cells that store more fat than normal. This research has the potential to lead to
new ways to think about therapies aimed at reducing the number of fat cells or altering
fat cell function in ways that reduce the complications of obesity, says Lazar.

Scientists can now measure how full or hungry a mouse feels, thanks to a new technique
which uses imaging to reveal how neurons behave in the part of the brain which regulates
appetite. Researchers hope the technique, which uses magnetic resonance imaging, will
enable a far greater understanding of why certain people become obese when others do not,
and why different people have different appetites.

Could the simple sugar responsible for putting the sweet in everything from bananas to
root beer be the missing link in understanding what puts the fat on a persons
thighs? Yes, according to a book penned by a University of Florida researcher that was
published today.In his book, The Sugar Fix: The High-Fructose Fallout That Is Making
You Fat And Sick, Dr. Richard Johnson reviews the increasing evidence that fructose
may play a role in the obesity epidemic and proposes a low-fructose diet he believes could
help people lose weight and potentially prevent diabetes and cardiovascular disease.

Scientists have acquired new insight into how the 'obesity gene' triggers weight gain in
some individuals. Their findings, reported online today in Science Express, could have
implications for the future treatment of obesity as well as adult-onset diabetes.

The health effects of obesity involve complex interactions between many body organs that
can obscure insight into underlying mechanisms. A more complete understanding of the
common underlying defects that occur at the cellular level might prove productive in
uncovering the causes and consequences of obesity.

Children who carry a gene strongly associated with obesity could offset its effect by
eating a low energy density diet, according to new research from UCL (University College
London) and the University of Bristol published today in PLoS ONE. The study, based on
data from a sample of 2275 children from the Bristol-based ALSPAC study (Children of the
90s) provides evidence that people might be able to avoid becoming obese if they adopt a
healthier diet with a low energy density  even those who carry the FTO gene,
identified as being a high risk gene for obesity. Dietary energy density (DED) refers to
the amount of energy consumed per unit weight of food, or number of calories per bite. A
low dietary energy density can be achieved by eating lots of water-rich foods like fruits
and vegetables and limiting foods high in fat and sugar like chocolate and biscuits. The
researchers looked at how DED affected the build up of fat in the body over a period of
three years in children aged between 10 and 13 years old. They found that children with a
more energy dense diet (more calories per bite) tended to have more fat mass three years
later and also confirmed that those carrying the high risk gene had greater fat mass
overall. When the researchers looked at whether children with the FTO gene had a stronger
reaction to an energy dense diet than children with a lower genetic risk they found that
they did not. These results indicate that if a child with a high genetic risk eats a diet
with fewer calories per bite, they may be able to offset the effect of the gene on weight
gain and so stay a healthy weight.

Scientists can now measure how full or hungry a mouse feels, thanks to a new technique
which uses imaging to reveal how neurons behave in the part of the brain which regulates
appetite. Researchers hope the technique, which uses magnetic resonance imaging, will
enable a far greater understanding of why certain people become obese when others do not,
and why different people have different appetites. The new study, led by researchers from
Imperial College London, is described in a paper published today in the Journal of
Neuroscience. It had previously been very difficult to measure satiety, which is the
psychological feeling of being full and satisfied rather than physical fullness. To judge
satiety scientists have relied on asking volunteers in trials how full they feel, or
watching how much food is eaten, rather than using more objective measures.

Is one diet as good as another? U
of I study says no and tells you why

Any diet will do? Not if you want to lose fat instead of muscle. Not if you want to lower
your triglyceride levels so you'll be less likely to develop diabetes and heart disease.
Not if you want to avoid cravings that tempt you to cheat on your diet. And not if you
want to keep the weight off long-term. "Our latest study shows you have a better
chance of achieving all these goals if you follow a diet that is moderately high in
protein," said Donald Layman, a University of Illinois professor emeritus of
nutrition. The research was published in the March Journal of Nutrition. Layman's new
study followed the weight-loss efforts of 130 persons at two sites, the U of I and Penn
State University, during 4 months of active weight loss and 8 months of maintenance. Two
previous studies had looked at short-term weight loss; this one was designed to look at
long-term effects, he said. Although both plans were equal in calories, half the group
followed a moderate-protein diet (40% carbohydrates, 30% protein, 30% fat) while the other
followed a diet based on USDA's food-guide pyramid (55% carbohydrates, 15% protein, 15%
fat). "Persons in the first group ate twice the amount of protein as the second
group," said Layman. And the difference in protein made all the difference in
improved body composition and body lipids, he said.

Lower thyroid activity tied to weight gainMiddle-aged adults whose thyroid gland is mildly
underactive, but still functioning in the normal range, may be more prone to weight gain,
a new study suggests. The thyroid is a gland in the neck that produces hormones that
regulate the body's metabolism. In a disorder called hypothyroidism, the gland is
underactive, causing symptoms such as fatigue, sensitivity to cold, dry skin and weight
gain.

Adults who eat apples, apple juice and applesauce have a significantly reduced risk of
metabolic syndrome, a cluster of health problems that are linked to numerous chronic
diseases such as diabetes and cardiovascular disease.

The study, which looked at the long-term effectiveness of anti-obesity medications, found
that three drugs recommended for long-term use -- orlistat, sibutramine and rimonabant --
reduced weight by less than 5 kg (11 pounds). This equated to a loss of less than 5
percent of total body weight. Guidelines from the National Institute for Clinical
Excellence recommend stopping the use of anti-obesity drugs if 5 percent of total body
weight is not lost after three months.

The cells lining blood vessels are known to be important for maintaining health, but
researchers at the Indiana University School of Medicine believe these cells may perform
an unsuspected task -- controlling the development of fat cells. Their findings are
reported in the September issue of the journal Stem Cells. The researchers found that
precursor or stem cells have a markedly reduced tendency to develop into fat cells when
placed in direct contact with healthy endothelial cells, which are the cells that line
blood vessels.

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Researchers note differences between people and animals on calorie restriction

calorie restriction, a diet that is low in calories and high in nutrition, may not be as
effective at extending life in people as it is in rodents, according to scientists at
Washington University School of Medicine in St. Louis. Previous research had shown that
laboratory animals given 30 percent to 50 percent less food can live up to 50 percent
longer. Because of those findings, some people have adopted calorie restriction in the
hope that they can lengthen their lives. But the new research suggests the diet may not
have the desired effect unless people on calorie restriction also pay attention to their
protein intake.

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Monell Researchers Find Metabolic Defect in Liver That Can Lead To Obesity

Researchers at the Monell Center have identified a genetically-transmitted defect that can
lead to obesity. The defect may explain why some people become obese while others remain
lean. The findings could open the door to the development of new drugs to curb appetite
and promote weight loss.

afslanken
Research team discovers brain pathway responsible for obesity

University of Wisconsin-Madison researchers, for the first time, have found a messaging
system in the brain that directly affects food intake and body weight.Reported in the Oct.
3 issue of Cell, the findings - from a study in mice - point to a completely new approach
to treating and preventing obesity in humans. The discovery also offers hope for new ways
to treat related disorders, such as type 2 diabetes and cardiovascular diseases - the most
prevalent health problems in the United States and the rest of the developed world. Led by
Dongsheng Cai, an assistant professor of physiology at the UW-Madison School of Medicine
and Public Health, the researchers looked specifically at the hypothalamus - the brain
structure responsible for maintaining a steady state in the body - and for the first time
found that a cell-signaling pathway primarily associated with inflammation also influences
the regulation of food intake. Stimulating the pathway led the animals to increase their
energy consumption, while suppressing it helped them maintain normal food intake and body
weight. The research stems from recent explorations into the problem called metabolic
inflammation, a byproduct of too much food or energy consumption. Unlike the classical
inflammation typically observed in infections, injuries and diseases such as cancer, the
metabolic inflammation seen in obesity-related diseases is much milder, doesn't lead to
overt symptoms or cause tissues damage. "Metabolic inflammation is a chronic,
low-grade condition consisting of inflammatory-like responses at the molecular level. It
has many downstream consequences," says Cai. "It causes cellular dysfunction,
which can decrease the regulation of several physiological processes, including
metabolism." Scientists believe that metabolic inflammation may be at the core of
many chronic, obesity-related metabolic disorders that are so common today, he adds. Cai
and his team zeroed in on NF-kappaB, a protein complex that can be activated specifically
by IKKbeta to induce inflammatory reactions in many cell systems.

A vegan diet was associated with significantly greater weight loss than the NCEP diet at 1
and 2 years. Both group support and meeting attendance were associated with significant
weight loss at follow-up.

Researchers from the Monell Center have for the first time attempted to count the number
of genes that contribute to obesity and body weight. The findings suggest that over 6,000
genes -- about 25 percent of the genome -- contribute to help determine an individual's
body weight. This high degree of complexity suggests that a quick fix to the obesity
problem is unlikely.

A vigorous 60-minute workout on a treadmill affects the release of two key appetite
hormones, ghrelin and peptide YY, while 90 minutes of weight lifting affects the level of
only ghrelin, according to a new study. Taken together, the research shows that aerobic
exercise is better at suppressing appetite than non-aerobic exercise and provides a
possible explanation for how that happens. This line of research may eventually lead to
more effective ways to use exercise to help control weight, according to the senior
author, David J. Stensel of Loughborough University in the United Kingdom. The study,
The influence of resistance and aerobic exercise on hunger, circulating levels of
acylated ghrelin and peptide YY in healthy males, appears in the online edition of
The American Journal of Physiology-Regulatory, Integrative and Comparative Physiology,
published by The American Physiological Society. The authors are David R. Broom, James A.
King and David J. Stensel of Loughborough University, and Rachel L. Batterham of
University College, London.

A research team from Universite Laval's Faculty of Medicine and Robert-Giffard Hospital
has demonstrated that weight gain induced by the use of antipsychotic drugs -- which in
extreme cases can be as high as 30 kilos in only one month -- can be avoided through a
specially designed weight control program. The researchers report the details of their
findings in a recent edition of the Australian and New Zealand Journal of Psychiatry.

A previously unknown mutation discovered in a common roundworm holds the promise of new
treatments for obesity in humans, McGill University researchers say. Their study was
published Dec. 3 in the journal Nature, and was funded by the Canadian Cancer Society and
the Canadian Institutes of Health Research. In lean times, a normal Caenorhabditis elegans
worm goes into a form of suspended animation called "dauer" that slows its
metabolism and allows it to survive for extended periods without food. "When they go
into dauer, these worms radically alter their metabolism," said Dr. Richard Roy, a
cancer researcher at McGill's Department of Biology specializing in the control of cell
division. "They shut down everything energy-consuming, which includes foraging, cell
division and reproduction." Unlike other "hibernating" organisms, C.
elegans maintains a degree of mobility during dauer by stocking up on energy in the form
of fats  or lipids  which they store in special cells or reserves. "This
allows them to live up to six months without eating, instead of the two weeks they would
otherwise have," Roy explained. A worm with the newly discovered mutation, however,
will usually die within a week of going into dauer "These mutants somehow cannot shut
down the process of cell division, which is why we noticed them in the first place,"
Roy said. "However, that's not what kills them. They cannot adjust their metabolism
correctly. They store up their six-month lipid reserves, but as soon as they shift into
dauer they use them up within a few days. This is because they lack an enzyme that blocks
the activity of a very important triglyceride lipase. Without this regulation the lipase
burns up all the fat it encounters and destroys the worm's energy reserves."

In simple terms, individuals become obese if they eat more calories than they burn.
However, the molecular pathways that control feeding behavior and cellular energy
expenditure are highly complex and not completely understood. In a study that appears
online on August 9 in advance of publication in the September print issue of the Journal
of Clinical Investigation, Clay Semenkovich and colleagues from Washington University
School of Medicine, St. Louis, show that mice lacking a protein known as FAS in beta-islet
cells in the pancreas and in the region of the brain known as the hypothalamus are lean
because they eat less and move around more than normal mice. These effects on behavior
were associated with decreased signaling in the hypothalamus through a protein known as
PPAR-alpha. Administration of a PPAR-alpha agonist into the hypothalamus increased the
amount mice lacking FAS specifically in the beta-islet cells and in the hypothalamus ate
but did not increase the amount normal mice ate. This study therefore identifies
FAS-mediated activation of PPAR-alpha as a molecular pathway controlling feeding behavior
in mice.

Researchers at Columbia University Medical Center have now identified a surprising and
critically important novel function of the skeleton. They've shown for the first time that
the skeleton is an endocrine organ that helps control our sugar metabolism and weight and,
as such, is a major determinant of the development of type 2 diabetes. The research is
published in the Aug. 10 issue of Cell.

New research suggests that genes that predispose people to obesity act in the brain and
that perhaps some people are simply hardwired to overeat. An international research team
co-led by the University of Michigan found six new genes that help explain body mass index
and obesity, and all but one of the genes are tied to the brain rather than to metabolic
functions, such as fat storage and sugar metabolism. In addition to the six new genes, the
study also confirmed the role of two other genes previously associated with obesity, said
co-principal investigator Goncalo Abecasis, an associate professor at the U-M School of
Public Health. The study will appear online Dec. 14 in advance of print publication in the
journal Nature Genetics. It's significant that five of the six new genes also impact brain
function, because the findings suggest people could simply be programmed to overeat, said
U-M postdoctoral researcher Cristen Willer, first author on the study. The brain, she
said, has two main functions related to weight: appetite control and the regulation of
one's total energy balance (whether you burn more calories or conserve more energy).
"This research tells you a little about what kinds of drugs you want to develop and
where you want them to act," Abecasis said.

Researchers at Albert Einstein College of Medicine of Yeshiva University have found that
overactivity of a brain enzyme may play a role in preventing weight gain and obesity. The
findings were reported in Cell Metabolism. To understand what drives hunger and causes
metabolic disease, many scientists have focused on the hypothalamus, an almond-sized
structure located deep within the brain that controls body temperature, hunger, and
thirst. Specialized nerve cells in the hypothalamus sense whether the body contains
adequate amounts of nutrients and stored body fat. The cells then send out signals telling
other parts of the brain to adjust food intake, metabolic rates, and physical activity
accordingly  keeping the body's caloric intake in balance with calories burned. To
learn more about these nutrient-sensing pathways and how they go awry in metabolic
disorders, researchers at Einstein focused on an enzyme called p70 S6 Kinase 1, or S6K,
which plays a role in regulating the growth and proliferation of all cells, including
nerve cells.

Einstein researchers - Do national
dietary guidelines do more harm than good?

Researchers at Albert Einstein College of Medicine of Yeshiva University raise questions
about the benefits of federal dietary guidelines. The researchers, led by Paul Marantz,
M.D., MPH, associate dean for clinical research education at Einstein, outline their
argument in the Jan. 22 online edition of the American Journal of Preventive Medicine.

Saturday can be the worst enemy for our waistlines, according to researchers at the School
of Medicine. They found that study subjects on strict diet and exercise programs tend to
lose weight more slowly than expected because they eat more on weekends than during the
week

Another reason to avoid high-fat
diet  it can disrupt our biological clock

Indulgence in a high-fat diet can not only lead to overweight because of excessive calorie
intake, but also can affect the balance of circadian rhythms  everyones
24-hour biological clock, Hebrew University of Jerusalem researchers have shown. The
biological clock regulates the expression and/or activity of enzymes and hormones involved
in metabolism, and disturbance of the clock can lead to such phenomena as hormone
imbalance, obesity, psychological and sleep disorders and cancer. While light is the
strongest factor affecting the circadian clock, Dr. Oren Froy and his colleagues of the
Institute of Biochemistry, Food Science and Nutrition at the Hebrew Universitys
Robert H. Smith Faculty of Agriculture, Food and Environment in Rehovot, have demonstrated
in their experiments with laboratory mice that there is a cause-and-effect relation
between diet and biological clock imbalance. To examine this thesis, Froy and his
colleagues, Ph.D. student Maayan Barnea and Zecharia Madar, the Karl Bach Professor of
Agricultural Biochemistry, tested whether the clock controls the adiponectin signaling
pathway in the liver and, if so, how fasting and a high-fat diet affect this control.
Adiponectin is secreted from differentiated adipocytes (fat tissue) and is involved in
glucose and lipid metabolism. It increases fatty acid oxidation and promotes insulin
sensitivity, two highly important factors in maintaining proper metabolism.

A new implantable medical device, developed in collaboration with Mayo Clinic researchers,
shows promise as a reversible and less extreme alternative to existing bariatric
surgeries, according to findings published in the current issue of the journal Surgery.

Suspicion is growing that fructose -- found in fresh fruit, fruit juice and preserves --
is fueling the obesity epidemic. A US study has found that overweight adults who were
given large amounts of fructose in their diet had an alarming increase in intra-abdominal
fat -- which causes a pot belly and has been linked to an increased risk of diabetes and
cardiovascular disease. The study, announced at a meeting last week, did not find the same
results with a test group consuming glucose instead.

Research on the effects of the female sex hormone estrogen in the brain lend credence to
what many women have suspected about the hormonal changes that accompany aging: Menopause
can make you fat. In animal experiments, researchers showed how estrogen receptors in the
brain serve as a master switch to control food intake, energy expenditure and body fat
distribution. The study will be presented in August at the American Chemical Society
national meeting in Boston.

Common virus may contribute to
obesity in some people, new study shows

A common virus may cause obesity in some people, according to new evidence in a controlled
laboratory study. Scientists showed that infection with human adenovirus-36, long
recognized as a cause of respiratory and eye infections in humans, transforms adult stem
cells obtained from fat tissue into fat cells. The study, which might lead to new
treatments for obesity, will be reported in August at the American Chemical Society
national meeting in Boston.

Verhulst et al. investigated the association between body mass index (BMI) standard
deviation score and prenatal exposure to hexachlorobenzene,
dichlorodiphenyldichloroethylene (DDE), dioxin-like compounds, and polychlorinated
biphenyls (PCBs) in a random sample of motherinfant pairs living in Flanders,
Belgium. PCBs were associated with increased BMI during early childhood. Future studies
are needed to confirm the findings and to assess possible mechanisms by which these
pollutants could alter energy metabolism.

Obesity starts in the head? Six
newly discovered genes for obesity have a neural effect

Obesity is known to increase the risk of chronic disorders, such as diabetes (type 2). An
international team of scientists with German participation through the Helmholtz Zentrum
MŁnchen identified six new obesity genes. Gene expression analyses have shown that all
six genes are active in brain cells.

Cutting calories helps rodents live longer by boosting cells' ability to recycle damaged
parts so they can maintain efficient energy production, according to a University of
Florida Institute on Aging study. Understanding how the process works at the cellular
level in rodents could help scientists develop drugs that mimic the process in humans.

Mice exposed to low temperatures develop more blood vessels in their adipose tissue and
metabolise body fat more quickly, according to a new study from Karolinska Institutet.
Scientists now hope to learn how to control blood vessel development in humans in order to
combat obesity and diabetes. The growth of fat cells and their metabolism depend on oxygen
and blood-borne nutrients. A possible way to regulate the amount of body fat  in
order, for instance, to combat obesity  can therefore be to affect the development
of blood vessels in the adipose tissue. A team of researchers at Karolinska Institutet
have now demonstrated the rapid development of blood vessels in the adipose tissue of mice
exposed to low temperatures. This is followed in its turn by a transformation of the
adipose tissue from 'white' fat to 'brown' fat, which has higher metabolic activity and
which breaks down more quickly.

Physical Activity May not be Key to
Obesity Epidemic, Loyola Study Finds

A recent international study fails to support the common belief that the number of
calories burned in physical activity is a key factor in rising rates of obesity.
Researchers from Loyola University Health System and other centers compared African
American women in metropolitan Chicago with women in rural Nigeria. On average, the
Chicago women weighed 184 pounds and the Nigerian women weighed 127 pounds. Researchers
had expected to find that the slimmer Nigerian women would be more physically active. To
their surprise, they found no significant difference between the two groups in the amount
of calories burned during physical activity. "Decreased physical activity may not be
the primary driver of the obesity epidemic," said Loyola nutritionist Amy Luke,
Ph.D., corresponding author of the study in the September 2008 issue of the journal
Obesity. Luke is an associate professor in the Department of Preventive Medicine and
Epidemiology at Loyola University Chicago Stritch School of Medicine.Physical activity is
defined as anything that gets your body moving. U.S. government guidelines say that each
week, adults need at least 2 Ĺ hours of moderate aerobic activity (such as brisk walking)
or 75 minutes of vigorous activity (such as jogging). Adults also should do
muscle-strengthening activities, such as weight-lifting or sit-ups, at least twice a week.

The discovery more than a decade ago of leptin, an appetite-suppressing hormone secreted
by fat tissue, generated headlines and great hopes for an effective treatment for obesity.
But hopes dimmed when it was found that obese people are unresponsive to leptin due to
development of leptin resistance in the brain. Now, researchers at Children's Hospital
Boston report the first agents demonstrated to sensitize the brain to leptin: oral drugs
that are already FDA-approved and known to be safe. Findings were published January 7 by
the journal Cell Metabolism. In 1995, researchers reported in Science that they had
isolated a protein that is present in normal mice, but not in an obese strain of mice
called ob/ob, which lacked a gene also called ob. When either obese or normal mice were
directly injected with the protein  now called leptin  they ate less and lost
weight. "Everyone in the field thought they would get the Nobel," says Umut
Ozcan, MD, of Children's Division of Endocrinology. Unfortunately, when obese humans took
the hormone, they lost weight only temporarily  then rebounded back. "Most
humans who are obese have leptin resistance," says Ozcan. "Leptin goes to the
brain and knocks on the door, but inside, the person is deaf."

New evidence in mice bolsters the notion that a version of a gene earlier shown to protect
lean people against weight gain and insulin resistance can have the opposite effect in
those who eat a high-fat diet and are heavier, reveals a report in the January 7th issue
of the journal Cell Metabolism, a Cell Press publication. The findings suggest that the 12
percent of people who carry the so-called Ala12 version of the gene that serves as a
master controller of fat differentiation will be more sensitive than most to the amount of
fat in their diets. (That fat-moderating gene is called peroxisome proliferator-activated
receptor gamma isoform 2, or Pparg2.) The Ala12 gene variant in question is less active
and less efficient in driving fat cells' formation than the more common Pro12 version, the
researchers explained. As a result, individuals carrying Ala12 are generally less obese
and more sensitive to insulin, but that can change if they shift to a less sensible,
fat-laden meal plan. Genetic testing for the variant might therefore be used as a
diagnostic tool, said Johan Auwerx of Universitť Louis Pasteur in France and the Ecole
Polytechnique Fťdťrale de Lausanne in Switzerland. "Through dietary counseling,
carriers could be informed that they really need to watch out for high fat in their
diets," he said. The findings also raise a potential caution about the long-term
effects of drugs called thiazolidinediones (TZDs) now in use for the treatment of
diabetes, he added. Those drugs stimulate activity of the Pparg2 receptor. The findings
suggest it may be betterat least in some settingsto have a less active
receptor.

In obese individuals, fat cells are bloated and inflamed because they receive too many
nutrients, including lipids. In these cells, various components cannot work properly
anymore and, instead, they activate new proteins to cope with the situation. One of the
most challenged organelles in obese fat cells is a maze-like compartment called the
endoplasmic reticulum (ER) that makes proteins and lipid droplets and senses the amount of
nutrients that enter the cell. Margaret F. Gregor and Gokhan S. Hotamisligil review
current knowledge about how the ER works in fat cells and is modified in obesity. They
show that when a fat cell receives too many nutrients, the ER is overwhelmed and triggers
a process called the unfolded protein response (UPR). This process is one of many cellular
responses that activate proteins that increase inflammation and can even result in the
death of the cell. UPR also causes insulin resistance, a condition in which the production
and function of insulin  a hormone produced by the pancreas  is impaired and
blood sugar is too high. The scientists show that by better understanding how the ER
works, it may be possible to devise a therapy that enhances the function of the ER and
maybe improve the health of obese people. Already, two molecules that protect the ER from
obesity-related stress have shown some success in mice. Called PBA and TUDCA, the
molecules decreased blood sugar and insulin levels and improved overall response to
insulin production.

Researchers at the University of California, Berkeley, have identified a new enzyme that
plays a far more important role than expected in controlling the breakdown of fat. In a
new study to be published Jan. 11 in the journal Nature Medicine, researchers report that
mice that have had this enzyme disabled remained lean despite eating a high-fat diet and
losing a hormone that suppresses appetite."We have discovered a new enzyme within fat
cells that is a key regulator of fat metabolism and body weight, making it a promising
target in the search for a treatment for human obesity," said Hei Sook Sul, UC
Berkeley professor of nutritional sciences and toxicology and principal investigator of
the research. Sul's research team includes the three co-lead authors of the paper, all
from UC Berkeley's Department of Nutritional Sciences and Toxicology: Kathy Jaworski,
former post-doctoral researcher; Maryam Ahmadian, graduate student; and Robin Duncan,
post-doctoral fellow. The enzyme in the spotlight, adipose-specific phospholipase A2
(AdPLA), is found in abundance only in fat tissue. AdPLA sets off a chain of events that
increases levels of a signaling molecule called prostaglandin E2 (PGE2), which suppresses
the breakdown of fat. Mice that have no AdPLA have lower PGE2 levels and a higher rate of
fat metabolism. "When levels of PGE2 are decreased because of the lack of AdPLA, fat
breakdown proceeds unchecked, resulting in leanness even in animals that eat all day
long," said co-lead author Duncan. In the study, mice that had the gene for AdPLA
expression knocked out were compared with a control group of normal mice. As soon as the
mice were weaned at about 3 weeks of age, researchers began offering the two groups of
mice an all-you-can-eat buffet of tasty, high-fat foods.

Scientists from Germany have recently discovered that extracts of a traditional herbal
remedy derived from Tabebuia impetiginosa can act to delay the absorption of dietary fat
in animal models. They believe that the extract could be incorporated into a food
supplement which may not only reduce obesity, but also lessen the risk of development of
type 2 diabetes and coronary heart disease.

An important new study from the Journal of Consumer Research explains the "American
obesity paradox": the parallel rise in obesity rates and the popularity of healthier
food. In a series of four studies, the researchers reveal that we over-generalize
"healthy" claims. In fact, consumers chose beverages, side dishes, and desserts
containing up to 131 percent more calories when the main dish was positioned as
"healthy."

It is obvious to most people that our health is affected by what we eat; now, however,
scientists have shown that it is also a matter of how often we eat. People who eat at
irregular times run a greater risk of developing insulin resistance and what is known as
metabolic syndrome, according to a study from the Swedish medical university Karolinska
Institutet. Metabolic syndrome is a condition whereby multiple risk factors for
cardiovascular disease and diabetes accumulate in one and the same individual. The chances
of developing the components of the syndrome  abdominal obesity, hypertension,
dyslipidemia, and glucose intolerance  are affected by several lifestyle factors, of
which diet is thought to be one of the most important. Scientists at Karolinska Institutet
have now, for the first time, showed that the frequency of meals, regardless of their
content, affects the chances of developing metabolic syndrome. The study, which was based
on a survey and medical examination of over four thousand 60-year old men and women, shows
that irregular eating is associated with a higher risk of metabolic syndrome.

Being overweight is a known risk factor for heart disease, diabetes and a host of other
health conditions. Now, a University of Georgia study published in the November issue of
the American Journal of Clinical Nutrition finds that obesity may also be bad for bone
health.

Doctors are not doing enough to pick up on problems with excessive weight loss, says a
Saint Louis University physician who helped draft recent guidelines to diagnose the
condition called "cachexia" (kuh-kex-ee-uh). "In sick people, weight loss
is an important indicator of disease and potentially impending death," said John
Morley, M.D., an endocrinologist and director of the division of geriatric medicine at
Saint Louis University School of Medicine. "Cachexia is an extraordinary problem for
people who are having other health problems, yet this is something that many physicians
don't pay attention to." A group of physicians and scientists agreed on a definition
of cachexia, which was published in the December edition of the medical journal, Clinical
Nutrition. "The definition is important because it gives physicians the guidelines to
make a diagnosis and treat the condition," Morley said. "A definition of
cachexia also makes it easier for scientists to conduct research and potentially develop
new therapies for the problem." About half of hospitalized patients and between 10
and 15 percent of sick patients who see a doctor have cachexia. The condition accompanies
diseases such as cancer, congestive heart failure, HIV, diabetes, kidney failure and COPD
(chronic obstructive pulmonary disease).

The scientists performed a 10-year follow-up study with healthy participants (206) aged
15-80 years at baseline in 1994, who participated in a nutrition survey in Valencia,
Spain. Data on diet, lifestyle factors, and body weight were obtained in 1994 and 2004
using a food frequency questionnaire (FFQ) and direct measurements. The average WG over
the study period was 3.41 kg. The data analysis of this study was limited by the number of
participants. The researchers did not perform separate analyses for men and women and
groups for statistical reasons (lack of sufficient statistical power). Concerning gender
differences there are some studies which have demonstrated different associations between
food group intake and weight changes among men and women. In conclusion, the researchers
found that increased fruit and vegetable intake was associated with significantly lower
risk of a medium WG (3,41 kg) over 10 years among adults of a Spanish Mediterranean
population. Dietary strategies to increase fruit and vegetable intake to prevent and
control overweight and obesity should be promoted more vigorously. The researchers
concluded that dietary patterns associated with a high intake of fruits and vegetables in
Mediterranean populations may reduce long-term risk of subsequent WG and obesity among
adults.

One of the reasons people on low-carbohydrate diets may lose weight is that they reduce
their intake of fructose, a type of sugar that can be made into body fat quickly,
according to a researcher at UT Southwestern Medical Center.

Dr. Troxler has invested hundreds of hours educating others about this Slow Starch Diet,
also known as the Low Glycemic Index Diet. His lectures are designed to teach people how
to eat low-glycemic index foods. Glycemic Index is a measure of how fast the starch we eat
changes into blood sugar. Slow starch has a low glycemic index and causes only a slow rise
in blood sugar.

New research links overeating and obesity with the brain system implicated in pleasure and
addictive behaviors strengthening the argument that obesity could be approached as an
addictive disorder. This is the first study to demonstrate that obesity predisposition is
associated with impairments in all mid-brain dopamine systems that are in place early in
postnatal life.

Study suggests 86 percent of
Americans could be overweight or obese by 2030

Most adults in the US will be overweight or obese by 2030, with related health care
spending projected to be as much as $956.9 billion, according to researchers at the Johns
Hopkins Bloomberg School of Public Health, the Agency for Healthcare Research and Quality
and the University of Pennsylvania School of Medicine.

The obesity epidemic may be linked to high worldwide rates of gum disease, according to a
new study conducted by researchers at Boston University and published in the journal
Proceedings of the National Academy of Sciences.

THE Japanese have had a reputation as the world leaders in business. Now a group of
Scottish businessmen have taken a leaf out of the books of their eastern counterparts
 to see if the Japanese diet and way of life improves their professional
performance.

Disrupted genetic regulation causes
common disturbance in metabolism of fat

The disease familial combined hyperlipidemia is a common cause of disturbed metabolism of
fat and early heart attacks. Swedish scientists have now developed a pioneering method and
can show for the first time what genes are regulated by the gene USF1, which is known to
cause the disease.

A predisposition for obesity might be wired into the brain from the start, suggests a new
study of rats in the February issue of Cell Metabolism, a publication of Cell Press.Rats
selectively bred to be prone to obesity show abnormalities in a part of the brain critical
for appetite control, the researchers found. Specifically, the researchers show that the
obese rats harbor defects in neurons of the arcuate nucleus (ARH) of the hypothalamus,
which leaves their brains less responsive to the hunger-suppressing hormone leptin.
The neurodevelopmental differences in these animals can be seen as early as the
first week, said Sebastien Bouret of the University of Southern California.
The results show that obesity can be wired into the brain from early life. The
three-million-dollar question now is how to get around this problem.

Scientists measure connection
between the built environment and obesity in baby boomers

Results showed significant associations among built-environment factors and the prevalence
of overweight/obesity and various forms of physical activity in middle-aged and older
adults. These findings suggest the need for public health and city planning officials to
consider how modifiable neighborhood-level, built-environment characteristics can create
more livable residential communities and promote active, healthy lifestyles.

Neuroscience researchers demonstrate for the first time that brain-derived neurotrophic
factor is an essential component of neural circuits which regulate body weight in adult
mice and that its expression in two particular brain regions is required to suppress
appetite.

The morbidly obese women and men had significantly lower concentrations of vitamin B-6,
vitamin C, 25-hydroxyvitamin D, and lipid-standardized vitamin E than did the healthy
controls (P <0.01 for each). The status of these vitamins was inadequate in a substantial proportion of the patients (11Ė38%). The status of vitamins A, B-1, B-2, and B-12 and of folic acid was adequate in most of the patients (95Ė100%). A moderately elevated C-reactive protein concentration was associated with lower vitamin A, B-6, and C concentrations. In a multiple regression analysis, concentrations of alkaline phosphatase (inverse relation) and vitamin C were the strongest determinants of serum vitamin B-6 concentrations.

A Human Hormone Blocker Is Found To
Help Prevent Obesity And Diabetes During Animal Testing

A new study finds that a chemical found in the body is capable of promoting weight loss,
improving insulin resistance and reversing diabetes in an animal model. The hormone is
gastric inhibitory polypeptide (GIP) receptor blockade.

A research team led by Mitchell Lazar, MD, PhD, Director of the Institute for Diabetes,
Obesity, and Metabolism at the University of Pennsylvania School of Medicine, has
discovered a key molecular partnership that coordinates body rhythms and metabolism. Lazar
and his colleagues, including the studys first author, Penn Veterinary Medicine
doctoral student Theresa Alenghat, studied a protein called NCoR that modulates the
bodys responses to metabolic hormones. They engineered a mutation into mice that
prevents NCoR from working with an enzyme that is normally its partner, HDAC3. These
animals showed changes in the expression f clock and metabolic genes, and were leaner,
more sensitive to insulin, and on different sleep-wake cycles than controls. The role of
the NCoR-HDAC3 partnership in regulating the bodys internal clock was previously
unknown. HDAC3 is an enzyme that affects gene expression by binding to receptors in the
cell nucleus to affect genes' activity, but not by directly changing DNA. The findings
suggest that HDAC via NCoR controls the bodys internal clock, and therefore
metabolism, through this epigenetic change. Their findings are reported in this
weeks issue of Nature. In the fight against the obesity and diabetes
epidemics, disruption of NCoR and its enzyme partner, might be a valuable new
weapon, says Lazar.

Obesity gradually numbs the taste sensation of rats to sweet foods and drives them to
consume larger and ever-sweeter meals, according to neuroscientists. Findings from the
Penn State study could uncover a critical link between taste and body weight, and reveal
how flab hooks the brain on sugary food. "When you have a reduced sensitivity to
palatable foods, you tend to consume it in higher amounts," said Andras Hajnal,
associate professor of neural and behavioral sciences at Penn State College of Medicine.
"It is a vicious circle." Previous studies have suggested that obese persons are
less sensitive to sweet taste and crave sweet foods more than lean people. However, little
is known about the specific differences between obese and lean individuals in their sense
of taste and the pleasure they derive from sweet foods. Hajnal and his Penn State
colleague Peter Kovacs, a post-doctoral fellow, investigated these differences by studying
the taste responses of two strains -- OLETF and LETO rats. Compared to the lean and
healthy LETO rats, the taste responses in OLETF rats mirror those in obese humans. These
rats have normal body weight at first, but they tend to chronically overeat due to a
missing satiety signal, become obese and develop diabetes. The obese rats also show an
increased preference for sweet foods and also are willing to work harder to obtain sweet
solutions as a reward for their learning. "When you have excess body weight, the
brain is supposed to tell you not to eat more, or not choose high caloric meals" said
Hajnal. "But this control apparently fails and thus the obesity epidemic is rising,
and we want to find out how the sense of taste drives up food intake."The researchers
implanted electrodes in the rodents' brains to record the firing of nerve cells when the
rats' tongues were exposed to various tastes -- salt, citric acid, plain water and six
different concentrations of sucrose.

Researchers have identified a molecule that tells your brain your stomach is full 
signaling that it's time to say no to a second piece of pumpkin pie and push back from the
Thanksgiving table. In studies with mice and rats, researchers have found that a chemical
messenger called NAPE is made in the small intestine after the animals ate a greasy meal.
After eating, NAPE  N-acylphosphatidylethanolamine, a mouthful in itself -- enters
the blood and travels to the brain, where it quashes hunger signals. Rats treated with
extra NAPE for five days ate less and lost weight, hinting that studying NAPE could help
researchers design better appetite suppressants or obesity drugs. Howard Hughes Medical
Institute investigator Gerald Shulman at Yale School of Medicine led the research team,
which reported its findings in the November 26, 2008, issue of the journal Cell. Shulman's
research group is well known for its work on understanding how insulin resistance develops
and leads to diabetes. In the course of that research, his team developed a sensitive
system to identify and measure lipids in tissue samples. After seeing the power of that
system in his diabetes research, Shulman was eager to see if it might also be applied to
understanding obesity. Some 300 million adults worldwide are severely overweight and at
risk for life-threatening illnesses such as type 2 diabetes and cardiovascular disease.
But obesity is difficult to treat. "We do not have good medical therapies for
obesity," Shulman says, noting that the small number of diet drugs on the market now
come with intolerable side effects and have only modest impacts on weight. "It's very
important to find other targets that might affect food intake." Despite many years
studying the physiology of appetite and hunger, researchers still do not have a clear
picture of how the brain keeps tabs on fat consumption. Fat is effective at satisfying
hunger, so Shulman and his colleagues at Yale and the University of Cincinnati decided to
see if they could find out whether the brain senses lipid intake directly. If they could
learn how that happens, they suspected, their findings might point toward a new treatment
for obesity. The team used Shulman's lipid analysis system to investigate what happens to
fat that enters the blood after ingesting a high-fat meal. The scientists reasoned that
the fat derivatives that enter the bloodstream might themselves serve as messengers to
signal the brain that the body has been fed. They used this approach to compare the lipids
present in blood plasma from rats that had fasted or eaten, and they zeroed in on
NAPE.They found only low levels of NAPE in the blood of rats that had fasted for 12 hours.
The level of NAPE shot up 40 to 50 percent in animals that had dined on high-fat chow.
Furthermore, NAPE didn't increase in rodents that ate only protein or carbohydrate,
suggesting that NAPE levels reflect the amount of fat eaten in a meal.

In the battle against obesity, Yale University researchers may have discovered a new
weapon  a naturally occurring molecule secreted by the gut that makes rats and mice
less hungry after fatty meals. The findings are published in the Nov. 26 issue of the
journal Cell. The report suggests the molecule may help regulate how much animals and
people eat, according to the team headed by Gerald I. Shulman, Yale professor of medicine
and cellular & molecular physiology and a Howard Hughes Medical Institute
investigator. Shulman's team studied a family of lipids called
N-acylphosphatidylethanolamines, or NAPEs, which are synthesized and secreted into the
blood by the small intestine after fatty foods are eaten. The team found that mice and
rats injected regularly with NAPEs ate less food and lost weight. In addition, treatment
with NAPEs appeared to reduce the activity of "hunger" neurons in the brain
while stimulating activity in neurons that are believed to play a role in reducing
appetite. In the last two decades, scientists have made great inroads toward understanding
how the body communicates with the brain to control food intake. So far, hormones such as
leptin that act as regulators of this complex system have proved disappointing when tested
as potential weight-loss treatments in humans. The researchers are now planning to
investigate how the findings in the Cell paper apply to humans. They will first study
non-human primates to determine if NAPE concentrations increase in a similar fashion after
fat ingestion. Then, says Shulman, "If chronic NAPE treatment is well tolerated and
can cause weight loss by a reduction of food intake, we would have strong impetus to move
forward with human NAPE trials."

Adiponectin is a metabolic link
between obesity and bone mineral density

Researchers at the University of Toronto, faculty of medicine, Toronto, Canada, have
discovered that adiponectin, a protein secreted from adipocytes, is a metabolic link that
can explain, in part, the known positive relationship between obesity and both bone
mineral density and reduced susceptibility to fractures.

How Do Individuals React to
Metabolic Stress? - Genetic Variation in Metabolism Identified

Metabolic diseases  in particular the increasingly prevalent type 2 diabetes 
are caused by a complex interaction between genetic disposition and unfavorable lifestyle,
above all unbalanced diet and too little physical exercise. Researchers at the Helmholtz
Zentrum MŁnchen have now for the first time been able to show a relationship between the
genetic make-up of an individual and differences in his/her metabolism. The team of
Professor Karsten Suhre of the Institute for Bioinformatics and Systems Biology at the
Helmholtz Zentrum MŁnchen and the Ludwig-Maximilians Universitšt MŁnchen (LMU) and Dr.
Christian Gieger and Thomas Illig of the Institute for Epidemiology in cooperation with
the Innsbruck company Biocrates Life Sciences AG determined the blood test results of
several hundred metabolites synchronously with more than 100 000 DNA variants (SNPs) of
284 adult test subjects. Their research was based on blood samples of participants of the
population-based KORA study (Kooperative Gesundheitsforschung in der Region Augsburg
[Cooperative Health Research in the Region of Augsburg] which is headed by Professor
H.-Erich Wichmann).

Researchers at the US Department of Energy's Brookhaven National Laboratory have found new
clues to why some people overeat and gain weight while others don't. Examining how the
human brain responds to "satiety" messages delivered when the stomach is in
various stages of fullness, the scientists have identified brain circuits that motivate
the desire to overeat. Treatments that target these circuits may prove useful in
controlling chronic overeating.

A persistent pollutant, tributyltin, has effects on gene activity in a wide range of
animal species at concentrations of parts per billion. Tributyl tin and its chemical
relatives bind to nuclear receptors that in turn activate genes influencing the formation
of fat storage cells. This and other evidence suggests a possible role for tributyl tin in
the obesity epidemic.

Diet may regulate obesity health
risks, but genes decide, says new research

The risk of obese people developing the metabolic syndrome that leads to diabetes,
hypertension, and heart disease, can not be solved by a one-size-fits-all diet programme,
according to new scientific findings. The results of Lipgene, a five year EU research
programme, show that personalised nutrition diets based on peoples genetic make-up will be
the way of the future when tackling obesity and its associated health risks. Currently,
obesity costs the EU an estimated 32.8 billion each year. And, at current rates, it
is estimated that 50% of Europeans will be obese by 2050. Obesity results when excess
calories are consumed and insufficient energy is spent (physical inactivity). Obesity is a
major health hazard worldwide, it is directly linked to several common diseases such as
diabetes, hypertension, heart disease, and some cancers. We analysed the findings
from 500 volunteers across Europe who took part in a dietary programme to measure the
effects of different diets on the development of the metabolic syndrome associated with
obesity, says Professor Helen Roche from the Institute of Food and Health at
University College Dublin, one of the principal scientists on the Lipgene programme.

Parathion and other organophosphate pesticides, the most widely used class of
insecticides, have long been known as neurotoxicants but were only recently linked to
metabolic disorders. A new study adds to the growing evidence that parathion may be
contributing to epidemics of obesity and diabetes.

Apple or pear shape is not main
culprit to heart woes  it's liver fat

For years, pear-shaped people who carry weight in the thighs and backside have been told
they are at lower risk for high blood pressure and heart disease than apple-shaped people
who carry fat in the abdomen. But new findings from nutrition researchers at Washington
University School of Medicine in St. Louis suggest body-shape comparisons don't completely
explain risk. In two studies, they report excess liver fat appears to be the real key to
insulin resistance, cholesterol abnormalities and other problems that contribute to
diabetes and cardiovascular disease. Having too much fat stored in the liver is known as
nonalcoholic fatty liver disease.

In addition to its strong associations with hypertension, cardiovascular disease, and
diabetes, pediatric obesity may induce alterations in thyroid function and structure,
according to a new study accepted for publication in The Endocrine Society's Journal of
Clinical Endocrinology & Metabolism (JCEM). Thyroid hormones drive metabolism, however
demonstration of a direct or strong correlation of obesity with deficient thyroid function
has been controversial, and previous studies provide conflicting conclusions. While some
studies have found that thyroid disorders may lead to obesity, this recent study shows
that in some cases, it is the obesity that may cause the disorder. "Our study shows
that alterations in thyroid function and structure are common in obese children and we may
have uncovered the link," said Giorgio Radetti, M.D., of the Regional Hospital of
Bolzano in Italy and lead author of the study. "We found an association between body
mass index and thyroid hormone levels which suggests that fat excess may have a role in
thyroid tissue modification." This study evaluated 186 overweight and obese children
over a period of nearly three years. Researchers measured subjects' thyroid hormone levels
and thyroid antibodies and also performed a thyroid ultrasound. The presence of thyroid
antibodies would suggest a diagnosis of Hashimoto's thyroiditis, an autoimmune disease of
the thyroid where T-cells attack the cells of the thyroid. In this study, 73 children did
not show these antibodies, yet their ultrasound pattern was still suggestive of
Hashimoto's thyroiditis.

After you eat a burger and fries or other fat-filled meal, a protein produced by the liver
may send a signal that fat is on the way, suggests a report in the December issue of the
journal Cell Metabolism, a Cell Press publication. Researchers have found in mice that the
liver produces a protein called adropin, which rises in response to high-fat foods and
falls after fasting. The protein seems to play a role in governing the activity of other
metabolic genes, particularly those involved in the production of lipids from
carbohydrates. Studies of the protein in obese animals suggest that it also plays a role
in insulin response and in preventing the buildup of fat in the liver (a condition known
as nonalcoholic fatty liver disease), the researchers said."What is remarkable is
that it appears that this factor is specifically regulated by the fat content of the
diet," making it one of the first such factors ever discovered, said Andrew Butler of
Pennington Biomedical Research Center, part of the Louisiana State University System. (The
findings follow another report in the November 26th issue of the journal Cell of a
phospholipid produced by the gut that rises after a fatty meal, signaling the brain to eat
less.) The new results suggest that treatments designed to deliver adropin or otherwise
boost its levels may hold promise in the war against obesity and associated metabolic
disorders, including fatty liver disease and type 2 diabetes. Indeed, Butler's team found
that animals that become obese after eating a high-fat diet for a period of 3 months or
due to a genetic mutation don't produce adropin normally. However, obese animals that are
manipulated to produce excess adropin or that are given the protein show less fat in their
livers and become more responsive to insulin. The mice also ultimately eat less and lose
weight, but the other metabolic improvements do not depend on the animals' shrinking
waistlines, Butler said.